Children Of Alcoholics

How Far Have We Come In Understanding this “Spiritual Malady” of Alcoholism?

In our previous blog we wondered if some commentators, who have co-occurring disorders may be puzzled at how having a “spiritual malady” could be related in any way to have a co-occurring condition?

This is a pretty valid question?

In fact this may be at the heart of the issue in many cases  of feeling the need to take medication  for so-called co-occurring conditions?

Seeing alcoholism as partly the product of a spiritual malady, instead of the affective disorder I believe it to be, may influence certain AAs to seek additional help for supposed additional conditions when the manifestation of these conditions may actually be part of the emotional disorder of alcoholism?

It is at least worth considering?

For me sometimes there is a confusion with what is perceived to be a spiritual malady?

I do not believe I have the same type of spiritual malady as my wife for example who is an normie, earthling, normal person (whatever that is?) I believe, if any thing I have a super enhanced, at times turbo-charged,  spiritual malady, often fuelled by stress/distress, as the result of my alcoholism.

I do not believe I have the same spiritual malady as other normal people such as those people who were in the Oxford Group.

That is not to say that normal people cannot be full of sin –  a cursory look around the work and it’s events will soon confirm this is the case. What I am saying is that they do not have the emotion dysregulation or fear based responding that I seem to have which often prompts “sin”.

By sin I mean negative emotions that cause distress to me and others.

For example, false pride, intolerance, impatience, arrogance, shame, lust, gluttony, greed. Yes these all create distress.

The spiritual principles of AA and the 12 steps in particular were drawn from the 4 absolutes of the Oxford group, via initially the 6 steps  and the idea of a spiritual malady is also borrowed from the Oxford group.

I have for several years wondered if the spiritual malady described in the Big Book adequate or accurate enough in describing what I suffer from.

I believe others have difficulties in reconciling the spiritual malady of the Big Book with their own alcoholism, addiction and  co-occurring conditions?

Part of the problem may lie in not being specific enough about what   alcoholism is.

It may be that research and the world have not progressed far enough to give a comprehensive account of what alcoholism is. Also the spiritual malady concept of AA has for 80 years helped millions of people recover from this most profound of conditions? So why change it if it’s not broke?

That is a good point? I am not advocating changing anything, I hope AA recovery remains as it is for 80 more years and much more years. I would not change one word in the first 164 pages of the BB.

However, many AAs ignore the spiritual malady thing completely, or do not do the steps, so, in my opinion, they often do not properly understand what they suffer from?

The magic of the the steps is that they seem to reveal  the patterns of behaviour that our actions have prompted over the course of our lives.  Maladaptive behaviours I should add. It helps us see ourselves and our condition of alcoholism and how it effects us and others.

It shows the areas of behaviour and attitudes that can be treated by working the steps. It shows us how our approach to life can possibly be transformed for the better.

For me personally it often showed a pattern of emotional responding to events that do not go my way!!?

As Bill Wilson once wrote we suffer when we cannot not get what we want or others seem to prevent us getting what we want.

My inventory of steps 4/5 showed me that my long lists of resentments were mainly the product of emotional immaturity and responding in an immature manner to not getting my way.

My inventory showed me also that I did not seem to have the facility previously to emotionally respond to the world in a mature way. As the world dominated me.

My recovery has thus since been about “growing up” a bit, however unsuccessful I am in this pursuit on occasion.

I have often written that this inherent emotional immaturity may even be linked to the possibility that the areas of my brain that regulate emotions have not matured properly  as alcoholic seem to have different connectivity, functionality and morphology (size/volume)  in this emotion regulation  circuit/network to healthy normal people.

Alcoholics seem not to be able to fully process emotional information externally, i.e reading emotion expression of faces accurately, or internally reading what emotions we are having, or even whether we are hungry or tired!

So we have issues with emotions and somatic/body feeling states. This is perhaps compounded by most of us having experienced abuse or maltreatment which can also lead to alexithymic characteristics such as not being able to label or describe, verbally, emotional states we are experiencing – although we can be good at intellectualising these emotions – which is not the same as processing them.

Alcoholics and children of alcoholics have a tendency to avoid emotions (use avoidant coping strategies) in fact and to use emotional reasoning when arguing a point.

These emotion processing deficits also appear to make us more impulsive, and to choose lesser short term gain over greater long term gain in decision making. It can lead to a distress feeling state that can make us fear based, perfectionist, have catastrophic thoughts, intolerance of uncertainty, low frustration and distress tolerance, be reactionary, moody, and immature in our emotional responding.

But how has any of this got anything to do with the so-called spiritual malady we are suppose to suffer from?

I believe the spiritual malady mixed with the ancedotal evidence throughout the BiG Book hints at these emotional difficulties as being an intrinsic part of our alcoholism, “We were having trouble with personal relationships, we couldn’t control our emotional natures, we were a prey to misery and depression, we couldn’t make a living, we had a feeling of uselessness, we were full of fear, we were unhappy…”

It was 80 years ago, so our knowledge base has moved on greatly from when the Big Book was written. Hence I believe we should appreciate that this definition of our condition has been updated by research into emotions especially in the last 20 years.

I am happy to say a spiritual malady is what we suffer from, as the steps provide a solution to my emotion disorder by treating it as a spiritual malady but  I do not think it is the straightforward spiritual malady adopted by AA from the Oxford Group, mainly because in the majority of situations I do not choose to sin, the sinning seems to happen to me. In other words it is the consequence of my fear based condition, this affective disorder.

The Oxford Group explain a general spiritual malady that all people can have. I do not think alcoholics are like all people. We are human beings, but extreme versions of human beings. I believe, even when I try my best to be virtuous and holy, I could sin at the sinning Olympics for my country. I am that naturally good at it!

I sin so naturally, effortlessly  and usually without even trying. I believe my so-called defects of character are linked to my underlying emotional disorder of alcoholism.

Sins I believe are the poisoned fruit of fear, often  helped along in alcoholics by false pride, shame and guilt. These defects are related to me being an alcoholic, they are intrinsic to my condition.

In order to illustrate how I believe my spiritual malady is the consequence of my emotional disorder, called alcoholism/addiction first let’s  go back to where this idea of spiritual malady came from.

According to a wonderful pamphlet “What is the Oxford Group”   written by The Layman With a Notebook ” Sin can kill not only the soul but mind, talents, and happiness as surely as a malignant physical disease can kill the body…

Sin is a disease with consequences we cannot foretell or judge; it is as contagious as any contagious disease our bodies may suffer from. The sin we commit within this hour may have unforeseen dire consequences even after we have long ceased to draw living breath…

…Like physical disease Sin needs antiseptics to prevent it from spreading; the soul needs cleaning as much as the body needs it…

Unhappiness to us and others, discontent, and, frequently, mental and bodily ill health are the direct results of Sin.

…Morbidity of mind must affect the physical health. If we can be absolutely truthful to ourselves we can analyse our sins for ourselves and trace their mental and physical effects. Sins can dominate us mentally and physically until we are their abject slaves. We cannot get rid of them by deciding to think no more about them; they never leave us of their own accord, and unless they are cut out by a decided surgical spiritual operation which will destroy them, roots and all, and set us free from their killing obsession, they grow in time like a deadly moss within us until we become warped in outlook not only towards others but towards ourselves….”

One can see how this concept of sin disease or in other words spiritual malady could be and was applied to early AA and incorporated into the Big Book of AA.

However, it is equally stating, I believe, that alcoholics suffer from the same spiritual malady as other people but our spiritual malady has led to chronic alcoholism, this is the manner in which sin has dominated  “mentally and physically until we are their abject slaves”.

In fact the Big book’s first chapters look more at the manifestation of this malady, problem drinking,    than the malady.  It suggests that there is more than this malady, there is also a physical reason for alcoholism- an allergy (or abnormal reaction) to alcohol. So this is a departure from the Oxford Group as it clearly states that alcoholism is more than a spiritual malady.   It is not simply the consequence of this spiritual malady although this malady may contribute.  So is this saying some of us are spiritually ill while also having an abnormal reaction to alcohol?

In the foreword The Doctor’s Opinion suggests  that “the body of the alcoholic is quite as abnormal as his mind.” and  a first mention of a disorder more than “spiritual” is suggested, “It did not satisfy us to be told that we could not control our drinking just because we were maladjusted to life, that we were in full flight from reality, or were outright mental defectives. These things were true to some extent, in fact, to a considerable extent with some of us. (my emphasis)

“The doctor’s theory that we have an allergy to alcohol interests us…as ex-problem drinkers, we can say that his explanation makes good sense. It explains many things for which we cannot otherwise account.”

“the action of alcohol on these chronic alcoholics is a manifestation of an allergy; that the phenomenon of craving is limited to this class and never occurs in the average temperate drinker.”

Here we have an abnormal reaction to alcohol and for some alcoholics a maladjustment to life.

For me this maladjustment to life is not exactly the same as the spiritual disease mentioned in the Oxford Group pamphlet.

All of my academic research in the last 6 years has explored the possibility that this “maladjustment to life” is more than a spiritual malady, i.e. it is not simply the consequence of Sin but the result of abnormal responding, emotionally (which has obvious consequences for sinning) to life.

This emotion dysregulation, as I name it, has consequences for how we feel about ourselves, how we interact with people, how much we feel we belong, how rewarding alcohol and drugs are, how much these substances make us feel better about ourselves (fix our feelings ) and how they turn off the internal critic of maladaptive and negative self schemas.

 

In fact our first “spiritual” wakening was probably the result of drinking as it transformed how we felt about ourselves and the world in which we lived. I know it did for me. In fact, I felt “more me” when I drank, it was like I escaped a restrictive sense of self to be a more expansive, people loving self.  I had a connection with the world I could not generate myself, when sober.

I was a “spirit awakening” if nothing else? It is interesting that a common definition of “spiritual” as it relates to AA, is a sense of connection with others.

As the BB states “Men and women drink essentially because they like the effect produced by alcohol. The sensation is so elusive that, while they admit it is injurious, they cannot after a time differentiate the true from the false. To them, their alcoholic life seems the only normal one. They are restless, irritable and discontented, unless they can again experience the sense of ease and comfort which comes at once by taking a few drinks—”

For me this section is saying our emotion dysregulation leads to feelings of being “restless, irritable and discontented” which prompt a return to drinking.

The Doctor’s Opinion even offers some classifications of alcoholics “The classification of alcoholics seems most difficult, and in much detail is outside the scope of this book. There are, of course, the psychopaths who are emotionally unstable… the manic-depressive type, who is, perhaps, the least understood by his friends, and about whom a whole chapter could be written.”

This section would appear to be stating clearly that there alcoholics who have other (co-occurring) conditions or conditions appearing as co-occurring?

I contend that alcoholism is an emotional disorder which results in chemical dependency on the substance of alcohol. However in order to treat it we have to first contend with the symptomatic manifestation of this disorder, chronic alcohol use, as it is the most life threatening aspect of this disorder when we present our selves at AA.

What we used once to regulate negative emotions and a sense of self has eventually come to regulate our emotions to such an extent that any distress leads to the compulsive response of drinking. Alcoholics had become a compulsive disorder to relief distress not to induce pleasure.

The “spiritual malady” of the Oxford group seems enhanced in me, I believe I sin more than normal people because of my emotional immaturity and reactivity. My “loss of control” over drinking is also linked to emotion processing difficulties as it prompted  impulsive, uninhibited drinking.

This emotional immaturity is referenced throughout the Big Book I believe.

“… He begins to think life doesn’t treat him right. He decides to exert himself more. He becomes, on the next occasion, still more demanding or gracious, as the case may be. Still the play does not suit him. Admitting he may be somewhat at fault, he is sure that other people are more to blame. He becomes angry, indignant, self-pitying. ”

“Whatever our protestations, are not most of us concerned with ourselves, our resentments, or our self-pity? Selfishness—self-centeredness! That, we think, is the root of our troubles. Driven by a hundred forms of fear, self-delusion, self-seeking, and self-pity, we step on the toes of our fellows and they retaliate. ”

“So our troubles, we think, are basically of our own making. They arise out of ourselves…”

“…Our liquor was but a symptom…”

“Resentment is the ”number one“ offender. It destroys more alcoholics than anything else. From it stem all forms of spiritual disease, for we have been not only mentally and physically ill, we have been spiritually sick.”

For me this is saying that out of my emotion dysregulation  “stem all forms of spiritual disease”.

It then talks of the fear that “was an evil and corroding thread; the fabric of our existence was shot through with it. ”

The list of emotional difficulties continues throughout the Big book’s first 164 pages.

One of the earliest studies on AA members concluded that  they were linked in commonality by two variables, emotional immaturity and grandiosity! I would contend that grandiosity is a part of emotional immaturity. I also contend that our “maladjustment to life” is based on emotional immaturity which is in itself a function of emotion regulation and processing deficits.

A book titled Matt Talbot by Morgan Costelloe has cites this reference –  “American authorities on alcoholism hold that the following psychological traits are commonly found in alcoholics:

> 1. A high level of anxiety in interpersonal relations
> 2. Emotional immaturity
> 3. Ambivalence towards authority
> 4. Low frustration tolerance
> 5. Low self-esteem
> 6. Perfectionism
> 7. Guilt
> 8. Feelings of isolation”

The list is  almost word-for-word identical with one in Howard Clinebell’s
“Understanding and Counseling the Alcoholic” p 53 of the revised edition of 1968 (the original edition appeared in 1956), the only difference being that Clinebell included grandiosity and compulsiveness.

Years after the Big Book Bill Wilson wrote about this emotion immaturity in the guise of discussing emotional sobriety, for me what he is saying that our emotional difficulties are present in long term recovery and need to be addressed – in other words there is more to alcoholism than sinning and drinking. What we are left with after the steps is ongoing and underlying difficulties with living life on life’s terms because we are emotionally immature. This I believe also preceded our drinking, for many of us anyway?

For many recovering alcoholics this may be another unpalatable truth, that they have issues with emotional responding, with being emotionally mature. If further validation is required I suggest a frank conversation with  a loved one, wife, husband, child, parent, etc.

Here is what Bill Wilson wrote ” Those adolescent urges that so many of us have for top approval, perfect security, and perfect romance—urges quite appropriate to age seventeen—prove to be an impossible way of life when we are at age forty-seven or fifty-seven.      Since AA began, I’ve taken immense wallops in all these areas because of my failure to grow up, emotionally and spiritually”. (my emphasis) 

Bill continues “Suddenly I realized what the matter was. My basic flaw had always been dependence – almost absolute dependence – on people or circumstances to supply me with prestige, security, and the like. Failing to get these things according to my perfectionist dreams and specifications, I had fought for them. And when defeat came, so did my depression.”

” Emotional and instinctual satisfactions, I saw, were really the extra dividends of having love, offering love, and expressing a love appropriate to each relation of life… I was victimized by false dependencies…       For my dependency meant demand—a demand for the possession and control of the people and the conditions surrounding me.”

For me this is emotional immaturity, regulating ones emotions and distress via external dependencies on others, demanding in an immature manner that others do one’s bidding?

I would suggest in relation to the issue of co-morbidities that one try to deal with these alcoholism related issues and then see if there are any other to deal with afterwards. For me, as someone who has been treated for anxiety and depression prior to recovery the 12 steps appear to have treated these as emotional consequences of my underlying condition of emotion dysregulation which I call alcoholism.

I think part of the issue is whether doctors, who know in my experience often know next to nothing generally about alcoholism,  can always properly diagnose depression and anxiety in someone suffering from alcoholism?

I also think the issues are complicate because alcoholism have some many similarities to GAD, MDD, OCD, and so on. They all may be similar but different.

This is why we need a satisfactory definition of what alcoholism and addition is? Rather than describing these conditions in terms of the manifest symptoms, i.e chronic substance abuse or, at times, vague “spiritual maladies”.

For example, one variable I believe is slightly different in alcoholism  to other affective disorders is distress based impulsivity which leads to maladaptive decision making, it leads to always wanting more of that…that anything.

These may be specific to addictive behaviours.

It may also be that we feel we have a co-occurring disorder because the underlying distress states prompt similar reactions in various differing disorders.

My distress feeds perfectionism, and catastrophic thinking as with other anxiety disorders like OCD, does that mean I have OCD too?

Maybe or maybe not? My tendency to not  regulate emotions has caused a distress state since childhood, it feeds into perfectionism and many other manifestations like always wanting just one more…?

It is the always wanting one more that makes my affective disorder that of addiction and not another disorder.

My affective disorder via various neural and cognitive – affective mechanisms leads to chronic substance use and dependency of these substances.

GAD, MDD, OCD have different manifestations and different mechanisms.

If we start by trying to recover from alcoholism and addiction and find we still have other issues then obviously address these with outside professional and specialist help.

I believe we can unwittingly complicate our treatment of alcoholism by believing we have (and treating) other conditions we see as distinct from alcoholism but which are in fact part of this condition called alcoholism.

I never fully knew what alcoholsim was until I did the 12 steps. Only then did it become clear what I suffered from?

I have suggested clearly in previous blogs how I think AA’s 12 recovery programme helps specifically with problems of emotion dysregulation.

How the Alcoholics Anonymous-12-step-program of recovery helps with emotional dysregulation

Maintaining Emotional Sobriety (and sanity) via the steps 10-12.

These illustrate how the 12 step programme can help with an emotion dysregulation disorder.

I end, however, with some words from a doctor who seems to be suggesting that AA works because it makes us more emotionally healthy.  For me she is saying how AA treats emotional illness.

An article by Dr. Jacqueline Chang’s paper given to the National Workshop for Health Liaison in York in 1998 and published in the Winter 1999 edition of the AA News suggests that

“The principles of the programme of Alcoholics Anonymous are scientific and closely follow all the helping therapies which lead people to emotional well-being.

AA proposes living “ One Day at a Time”. It is emotionally healthy to live in the day … in the here and now. Professional therapists teach people to live in the present.  AA encourages members to share their experience, strength and hope with other members. It is emotionally healthy to accept our past experiences, however painful, as past events and move on to a richer, more fulfilling future.

Step 1 in the AA programme is “ We admitted we were powerless over alcohol – that our lives had become unmanageable”. It is emotionally healthy to surrender and accept things over which we have no control.
“God grant us the serenity to accept the things we cannot change, courage to change the things we can and the wisdom to know the difference” is the Serenity Prayer used at every AA meeting. It is emotionally healthy to prioritise problems. The Serenity Prayer is the greatest exercise in prioritisation.

It is emotionally healthy to accept that we cannot change a particular situation but we can change the way we react to it.

It is emotionally healthy to accept yourself as you are.
It is emotionally healthy to recognise your environment and interact with it as it is, not as you wish it would be.  It is emotionally healthy to associate or be in contact with other human beings.

It is emotionally healthy to be altruistic – to help others without question or expectation.
It is emotionally healthy to anticipate – to plan for future discomfort or crises. This is the function of the AA Step programme. ”

 

AA provides many ways of becoming more emotionally well, which ultimately means more emotionally mature.

 

 

 

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.

Is the Impulsive Behaviour that Precedes Addiction Hardwired into the Brain?

In various blogs we have forwarded the idea that emotional and stress dysregulation are that the heart of addiction and alcoholism and are also possible present in those at risk to these disorders.

Essentially we suggest that the behavioural endpoint of addictive behaviours, the distress based impulsivity (negative urgency) seen in alcoholics and addicts which shapes decision making may be the consequence of chronic neurotoxic activity (as the consequence of chronic alcohol and drug use)  on brain areas which have a pre-existing impairments or vulnerability such as brain regions involved in emotional regulation, processing, inhibition and stress and reward response.

Here we cite an article (1) which looks at some of these brain regions, specifically those involved in emotional regulation and impulsivity and considers whether these deficits may be “hardwired” into the brain in terms of white and grey matter impairments.

 

Brain areas actively developing during adolescence include the prefrontal cortex, limbic system areas, and white matter myelin ( electrically insulating material that forms a layer, the myelin sheath – the yellow insulation below), usually around only the axon of a neuron. It is essential for the proper functioning of the nervous system.)

400px-Neuron_Hand-tuned.svg

These areas serving cognitive, behavioral, and emotional regulation may be particularly vulnerable to adverse alcohol effects.

Alternatively, deficits or developmental delays in these structures and their functions may underlie liability to accelerated alcohol use trajectories in adolescence.

The prefrontal cortex, limbic brain regions, white matter ( composed of bundles of myelinated nerve cell axons which connect various grey matter areas (the locations of nerve cell bodies) of the brain to each other (see below – grey on outside, white inside) and carry nerve impulses between neurons. Myelin acts as an insulator, increasing the speed of transmission of all nerve signals, and reward circuits undergo active development during adolescence (Chambers et al., 2003; Spear, 2000).

 

250px-Human_brain_right_dissected_lateral_view_description

 

These structures and their functions, involving behavioral, emotional and cognitive regulation, may be particularly vulnerable to the adverse effects of alcohol exposure during adolescence.

Delays or deficits in the development of neural substrates necessary for these psychological regulation abilities to fully develop may be termed neurodevelopmental dysmaturation.

download (6)

 

Psychological Dysregulation

The development of accelerated alcohol involvement in adolescence is not an isolated phenomenon, but is typically presaged by persistent behavioral characteristics including attentional deficits, conduct problems, and irritability (Chassin et al., 1999; Clark et al., 1997a, 2005; Tapert et al., 2002).

Two main psychological factors have been identified: (1) Behavioral Undercontrol, comprised of conduct disorder symptoms and personality characteristics including aggression and diminished constraint, and (2) Negative Emotionality, comprised of depression, anxiety and stress reactivity variables (Martin et al., 2000).

These two factors were significantly correlated. These correlated characteristics have been hypothesized to comprise the early phenotypic manifestations of a core liability for SUDs (Tarter et al., 1999).

The proposed construct manifested by these psychopathologic features has been termed psychological dysregulation (Clark and Winters, 2002). Psychological dysregulation is a deficiency in the ability to regulate attention, emotions and behavior in response to environmental challenges. Psychological regulation is thus the ability to modulate prepotent responses in order to optimize reward opportunities. The skills involved in psychological regulation include executive cognitive functioning (ECF), behavioral inhibition and emotional management.

Deficiencies in psychological regulation may be the result of delays or persistent deficits in the acquisition of behavioral, emotional, and cognitive regulation skills.

Adolescents at risk for developing SUDs exhibit deficits in psychological regulation. Childhood psychological dysregulation, or neurobehaviour disinhibition, correlates with parental substance use disorders (SUDs) and prospectively predicts adolescent alcohol and other substance use as well as related disorders (Clark et al., 2005; Tarter et al., 2003).

The psychological dysregulation dimension integrates several psycho patholological dimensions heretofore considered distinct, including affective disorders and SUDS themselves (Krueger et al., 2002).

Neurobiological Basis of Psychological Dysregulation

The functions subsumed under the construct of psychological dysregulation are thought to be served by the prefrontal cortex (Koechlin and Summerfield, 2007). The capabilities that comprise psychological regulation improve during adolescence (Levin et al., 1991; Welsh et al., 1991). The ongoing development of the prefrontal cortex has been hypothesized to be the primary neurobiological foundation for the advancement of these abilities (Happaney et al., 2004; Spear, 2000). Developmental abnormalities in the frontal cortex have been found in children and adolescents with behavioral problems reflecting psychological dysregulation (Rubia et al., 2000; Spear, 2000).

Diffusion tensor imaging (DTI) studies  indicated that white matter organization increases from early childhood to young adulthood (Klingberg et al., 1999; Nagy et al., 2004; Schmithorst et al., 2002; Zhang et al., 2005).White matter development may underlie advancing executive functioning. The prefrontal cortex is a brain region undergoing relatively late gray matter pruning, and volumes of gray matter appear to decrease over adolescence (Gogtay et al., 2004; Lenroot and Giedd, 2006; Sowell et al., 2001, 2004). Unlike grey matter volume, white matter volume appears to increase during adolescence, particularly in the prefrontal area (Ashtari et al., 2007;Barnea-Goraly et al., 2005; Lenroot and Giedd, 2006).

 

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White Matter Development and Alcohol Exposure

Selective white matter loss has been reported among adults with Alcohol Use Disorders (AUDs) (Carlen et al., 1978, 1986) and with fMRI (Agartz et al., 2003), and postmortem specimens (Krill et al., 1997).  Compared with controls, adolescents with AUDs have been found to have smaller prefrontal white matter volumes (DeBellis et al., 2005). Prefrontal grey and white matter volumes were compared in adolescents with AUDs. Compared with control subjects, subjects with AUDs had significantly smaller prefrontal white matter volumes.Marijuana use has also been found to be associated with smaller white matter volumes in adolescents (Medina et al., 2007b). While these volumetric findings suggest problematic frontal development among adolescents with AUD, the emergence of neuroimaging techniques developed to examine white matter organization may prove to be more specifically relevant to understanding the effects of alcohol on neurodevelopmental maturation.

Changes in gene expression may be involved in alteration of white matter structure in AUDs.  In a postmortem study, myelin-related genes were found to be down-regulated in the AUD group (Lewohl et al., 2000).

While evidence has been presented that alcohol consumption may disrupt white matter organization, the possibility remains that delayed or diminished white matter organization may presage alcohol involvement and constitute a risk factor for AUDs. Immaturity of white matter development and the related deficits in the functional integration of brain areas may in part explain individual differences in psychological regulation during adolescence. For example, disruptive behavior disorders in childhood, particularly conduct disorder, have been found to predict accelerated trajectories of alcohol use, cannabis use, and substance-related problems in adolescence (Clark et al., 1999).

Limbic System Development and Alcohol Exposure

The limbic system is central to the processing of affective stimuli, the successful formation of new memories, and the implementation of related responses. Limbic system structures, including the hippocampus and amygdala, may be susceptible to alcohol-induced dysmaturation.

Smaller hippocampal volumes have been reported in adults with AUDs compared with control adults (Sullivan et al., 1995). As hippocampal development progresses in adolescence (Gogtay et al., 2006), this brain area may be particularly susceptible to the adverse effects of alcohol involvement during this developmental period.

DeBellis et al. (2000) compared the hippocampal volumes of 12 adolescents and young adults with adolescent-onset AUD to those of 24 control subjects. Both left and right hippocampi were significantly smaller in AUD subjects compared to the volumes in controls. Specifically, left hippocampal volumes were smaller in teens with AUD than demographically similar controls, and youth with greater severity of AUD had the smallest left hippocampal volumes (Medina et al., 2007a; Nagel et al., 2005).

The amygdala may also be important for understanding the neurodevelopmental effects of alcohol exposure. The amygdala, along with ventral striatum, has been hypothesized to be involved in reward mechanisms and thereby critical for understanding alcohol use trajectories (Koob, 1999). Amygdala volumes have been found to be relatively smaller in high-risk older adolescents and adults with SUDs compared to that in control subjects (Hill et al., 2001; Makris et al., 2004). Lack of correlation with use levels has led to the suggestion that this may be a predisposing characteristics rather than a substance effect.

Interacting brain areas are involved in reward processing (McClure et al., 2004), motivation (Chambers et al., 2003), and decision-making (Verdejo-Garcia et al., 2006).  The interactions between the prefrontal cortex and subcortical areas, including the amygdala and nucleus accumbens, constitute the neurocircuitry involved in reward responding. In the affective component of reward responding, the amygdala appears to be a network node involved in reactivity to emotional stimuli (Hariri et al., 2006; Schwartz et al., 2003). An understanding of the adolescent development of neural circuits underlying reward processing and decision making is central to considering the role of these systems in the development of alcohol involvement.

Impulsivity, defined as acting without forethought, progressively decreases from childhood into adulthood. This change has been thought to occur as a result of neuromaturation in the prefrontal cortex (Casey et al., 2005).

The generation of behaviors optimizing long-term reward opportunities often involves behavioral inhibition. The activation of prefrontal cortical areas during response inhibition tasks has been found to increase from childhood through adolescence, a change corresponding to the development of abilities to suppress prepotent behaviors (Luna and Sweeney, 2004; Luna et al., 2004). The ability to select an optimally adaptive behavioral response while suppressing a predominant or prepotent response with problematic consequences defines impulse control and is fundamental to psychological regulation skills. Improved abilities in response inhibition and related prefrontal activation during adolescence are thought to involve maturation of functional connectivity subserved by ongoing myelination.

Adolescents with psychopathology predictive of SUDs, similar to adults with alcohol dependence, have difficulty with behavioral inhibition during laboratory tasks (Bjork et al., 2004a; Dougherty et al., 2003; Schweinsburg et al., 2004). Furthermore, adolescents with histories of substantial marijuana use, compared with control adolescents, showed more activation in frontal cortical areas during behavioral inhibition tasks (Tapert et al., 2007). More activitation suggests greater effort was required by the marijuana using group.

 

References

1.  Clark, D. B., Thatcher, D. L., & Tapert, S. F. (2008). Alcohol, psychological dysregulation, and adolescent brain development. Alcoholism: Clinical and Experimental Research, 32(3), 375-385.

 

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

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

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

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

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

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

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

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

 

Thoughtful little girl

 

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

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

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

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

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

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

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

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

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

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

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

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

 

References

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

 

Do alcoholics drive through life with Faulty Brakes!

There has been a lot of debate in the last thirty – forty years about genetic inheritance – with at least half of children of alcoholic families at risk for later alcoholism. What is less known is what exactly is inherited in our genes? What marks us out for later alcoholism? Prior to drinking are there aspects of our behaviour, personality or emotional responding that marks us out compared to so-called normal healthy types.

Recently research has looked at brain systems which overlap in decision making such as cognitive control over impulsive behaviour and also emotional processing. Children from alcoholics seem to have difficulties with both these overlapping circuits in the brain – they are not only impulsive but also do not seem to process emotions in the same way their “health” peers do. Research has also begun  to show that emotional processing is indeed important to making decisions, as is the ability to inhibit impulsive responses.

It seems  young alcoholics in the making, are not using our emotions  to make decisions and  are also prone to being impulsive. This difficulty with making decisions must shape all other future decisions ?

Youth for families with a history of alcoholism (FH+) are more likely to engage in early adolescent alcohol use (1), they may be more prone to experience the neurotoxic effects of alcohol use during adolescence.

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Heavy alcohol use during adolescence is related to poorer neuropsychological functioning, including response inhibition (2), working memory (3-5), and decision-making (6).

Neuroimaging studies have shown that alcohol abusing teens have atypical grey matter volume in the PFC (7,8), and subcortical structures, such as the hippocampus (9,10) OFC and the amgydala.

Further, they have reduced integrity of white matter pathways, in both long-range connections between frontal and parietal brain regions as well as in pathways connecting subcortical and higher-order brain areas (11,12).

FMRI studies have found reduced BOLD response in adolescent alcohol abusers
in brain regions important affective decision-making (13).

The raging debate in research has been to whether these deficits are a consequence of heavy alcohol use or if genetic and environmental factors, such as family history of alcoholism, may contribute.

Risk Factor for Alcohol Use Disorders (AUDs): Family History of Alcoholism

The observation that alcoholism runs in families has long been documented
(14-16). Over the past few decades, adoption (17,18) and twin (19)
studies have suggested that there is an increased likelihood of individuals with a family history of alcoholism to develop the disorder themselves (20, 21).

These studies indicate that familial alcoholism is one of the most robust predictors of the development of an AUD during one’s lifetime. Furthermore, this risk factor appears to be stable over time, since it also predicts the chronicity of alcohol dependence at multiple time points (22).
This indicates that higher familial density is often associated with greater
risk (23), with genetic vulnerability accounting for about 30-50% of
individual risk (24-26).

 

One of the best characterized findings in individuals with familial alcoholism are greater impulsivity and difficulties in response inhibition which are commonly seen in this population (27,28), and FH+ individuals are less able to delay reward gratification compared with their peers (29).

Emotional processing and its relationship with executive control has received much less
attention in FH+ individuals.

Alcohol Use Disorders and Emotional Processing

Emotion Recognition and Affective Processing – Research suggests that alcohol use disorder (AUDs)  are associated with deficits in emotion recognition
(30-33), which may be related to atypical brain structure and functioning observed in the
limbic system among alcoholics (34-37).

Alcoholics not only tend to overestimate the intensity of emotions seen in faces  but they also make more negative emotional attributions and often confuse one emotion for another, such as mislabeling disgust as anger or contempt (32). Additionally, these deficits seem to be specific to alcoholism, since alcoholics, both recently abstinent and long-term abstinent, perform poorer on emotion recognition tasks than individuals with other drug abuse history (38). Alcoholics have also been shown to have slower reaction time when recognizing emotions (39).
Furthermore, poorer accuracy on emotion recognition tasks in alcoholics does not improve across the duration of the task, even though better performance is seen over time with other drug abusers (38).

Polysubstance abusing adults, the majority of whom were alcohol abusers, showed emotion recognition deficits on angry, disgusted, fearful, and sad faces (40). Based on the evidence of emotion recognition deficits in alcoholics, it is necessary to determine whether similar difficulties are present in FH+ youth that could be disruptive to emotional functioning and may contribute to the ultimately higher prevalence of alcohol abuse in this population.

Ultimately we may be observing here external emotional processing difficulties in the same manner we observed “internal” emotional processing difficulties in those with alexithymia, the reduced ability to “read” internal emotions of which a majority of alcoholics appear to suffer.

In summary, alcoholics and children of alcoholic families appear to have both external, i.e. recognition of other people’s emotions as well as their own and these may relate to immature development of brain regions which govern emotional, processing, recognition and regulation, which appears to contribute greatly to the initiation and progression of alcohol abuse.

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In addition to emotional processing deficits, alcoholics have various structural
and functional abnormalities in affective processing brain regions. Studies of the limbic system have found reduced volume in subcortical structures, including the amygdala, thalamus, ventral striatum, and hippocampus among adult alcoholics (41,42). Alcoholics with smaller amygdalar volumes, are more likely to continue drinking after six months of abstinence (37).

Marinkovic et al. (2009) alcoholics exhibited both amygdalar and hippocampal hypoactivity during face encoding, and when recognizing deeply encoded faces, alcoholics had significantly reduced amygdalar activity to positive and negative emotional expressions compared with controls (35). These results help explain findings in behavioral studies of alcoholics that have found considerable evidence for emotion recognition deficits in this population.

Furthermore, during emotion identification, alcoholics showed comparable
performance to controls, but had reduced brain response in the affective division of the
anterior cingulate cortex (ACC) to disgust and sadness, with this lack of affective response to aversive stimuli believed to underlie disinhibitory traits in AUDs (36).

There is also evidence to suggest that non-alcohol abusing FHP individuals
share similar deficits in affective systems to alcohol abusers, including reduced
amygdalar volume, less amygdalar activity in response to emotional stimuli, and high
rates of internalizing symptoms such as anxiety and depression (37; 45-47).

Furthermore, research examining the relationship between emotional
processing and cognition has found that poor inhibition in individuals with co-morbid
substance and alcohol abuse is associated with atypical arousal in response to affective images (48), and affective measures in FH+ alcoholics also relate to deficits in executive functioning, e.g impulsivity (47).

This suggests that familial history of AUDs may put individuals at greater risk for problems with emotional processing and associated disruptions in executive functioning (47), which could, in turn, increase risk for alcohol abuse (49).

As we suggested previously, in relation to decision making profiles, in those at risk, those with alexithymia and also with cocaine addicts, decision making often involves more emotion expressive-motor areas of the brain like the caudate nucleus which is more of a “feel it-do it” type of reaction to decision making or a emotionally impaired or distress-based impulsivity. If there is a difficulty  processing emotions, these emotions can not be used as a signal to guide adaptive, optimal decisions. Decisions appear more compulsive and short term.

It may be this tendency to act now, rather than later,  that defines the vulnerability in FH+ children. It is like driving through life with faulty brakes on decision making, which sets up a chain of maladaptive choices such as alcohol abuse which then damages these affective based decision making regions of the brain even more, with increasing  deleterious consequences as the addiction cycle progresses until the endpoint of addiction of very limited choice of behaviour as emotional distress acts eventually as a stimulus response to alcohol use.  Emotional processing usurped by compulsive responding.

 

References

Main reference – Cservenka, A., Fair, D. A., & Nagel, B. J. (2014). Emotional Processing and Brain Activity in Youth at High Risk for Alcoholism. Alcoholism: Clinical and Experimental Research.

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