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.




How Mindfulness could help Recovery?

Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence.

Yesterday we looked a how low heart rate variability in alcoholics (active and in recovery) may influence self, emotion and stress regulation, and have a limited effect on impulsivity, and result in a “locked in” attention to alcohol-related cues, all of which have obvious consequences for relapse.

Here we cite and use excerpts from an article by Eric Garland et al (1) which addresses the effects of mindfulness  meditation on those with alcohol dependence.

Although Garland suggest mindfulness could be an alternative to other treatment and recovery programs, I suggest that it can be used most effectively with other treatment and recovery programs, e.g. with step 11 of 12 step programs.

I believe the consequence of emotion dysregulation  over many years of addiction leaves behind numerous unprocessed emotions which have not been consigned to long term memory and as a result float around the mind as resentments, shame and guilt based memories etc.

Emotion dysregulation has not allowed us to consigned them properly to the past (the so-called wreckage of the past) or long term memory and only an intensive process of emotional processing these e.g. via step 4 or 5 or via an alternative stock taking of our pasts seems to resolve this problem.

I know from my previous experience of intensive meditation involving various 10 day intensive courses and meditating on a very regular basis, before realising I am an alcoholic, would always result in relapse via the distress of the past being resurgent in my mind.

Some method of addressing all of these past behaviours, which invariably have hurt someone, need to be addressed and processed, even making amends to those hurt by our previous behaviours,  before we profoundly ease the distress of the past and help facilitate a greater recovery and more effective meditation practice.

Anyway, that’s my vies, on with the article…

“When attention is fixated on visual or olfactory alcohol cues, alcohol dependent individuals exhibit significant psychophysiological reactivity (Carter & Tiffany 1999). In turn, this alcohol cue-reactivity may lead to increased craving, which can trigger alcohol consumption as a means of reducing distress. Many persons recovering from alcohol use disorders attempt to suppress cravings, which, paradoxically, can serve to increase intrusive, automatic alcohol-related cognitions (Palfai, Monti, Colby, & Rohsenow 1997), dysphoria, and autonomic arousal (Wenzlaff & Wegner 2000). Indeed, among alcohol dependent persons, thought suppression is negatively correlated with vagally-mediated heart rate variability (Ingjaldsson, Laberg, & Thayer 2003), a putative index of emotion regulation and parasympathetic inhibition of stress reactions (Thayer & Lane 2000).

As thoughts of drinking intensify and are coupled with psychobiological distress, the impulse to consume alcohol as a form of palliative coping may overcome depleted self-regulation strength (Muraven, Collins, & Nienhaus 2002; Muraven & Shmueli 2006) leading to relapse. The attempt to avoid distress or allay its impact through compulsive alcohol consumption results in negative reinforcement conditioning that may perpetuate this cycle by further sensitizing the brain to future stressful encounters via allostatic dysregulation of neuroendocrine systems (Koob 2003). Components of this risk chain may be especially malleable to targeted behavioral therapies.

One such intervention, mindfulness training, which originates from Buddhist traditions but has been co-opted by Western clinicians, has recently gained prominence in the psychological and medical literatures for its salutary effects on stress-related biobehavioral conditions (Baer & Krietemeyer 2006; Ludwig & Kabat-Zinn 2008). Mindfulness involves self-regulation of a metacognitive form of attention: a nonreactive, non-evaluative monitoring of moment-by-moment cognition, emotion, perception, and physiological state without fixation on thoughts of past or future (Garland 2007). A growing body of research suggests that mindfulness affects implicit cognition and attentional processes (e.g., Jha, Krompinger, & Baime 2007; Lutz, Slagter, Dunne, & Davidson 2008; Wenk-Sormaz 2005) as well as heart rate variability indices of parasympathetic regulation (Tang et al. 2009).


Mindfulness treatments may enhance clinical outcomes in substance-abusing populations.

Bowen et al. (2007) found that mindfulness training of incarcerated inmates reduced post-release substance use, substance-related problems, and psychiatric symptoms to a greater extent than standard chemical dependency services offered at the prison. Other pilot studies of mindfulness-based interventions with substance abusers have found significant reductions in distress, negative affect, stress-related biomarkers, and substance use (Marcus, Fine, & Kouzekanani 2001; Marcus et al. 2003;Zgierska et al. 2008).

To that end, a randomized, controlled design was used to compare the therapeutic effects of a mindfulness-oriented recovery enhancement (MORE) intervention to those of an evidence-based alcohol dependence support group (ASG).

We hypothesized that, relative to ASG, MORE would result in significantly greaterdecreases in perceived stress, impaired alcohol response inhibition, craving for alcohol, psychiatric symptoms, and thought suppression and significantly greater increases in mindfulness and in heart rate variability (HRV) recovery from stress-primed alcohol cues.



Among recovering alcohol-dependent individuals, mindfulness training appears to be a potentially effective stress reduction technique. MORE reduced perceived stress to a greater extent than did ASG, which is noteworthy given that social support reduces stress reactivity and buffers deleterious effects of stressful life events (Christenfeld & Gerin 2000). The stress reduction effects of mindfulness training among nonclinical populations are well known in the literature (Grossman, Niemann, Schmidt, & Walach 2004), but it is notable that significant effects were obtained in a sample of clinically-disordered, alcohol-dependent adults with extensive trauma histories who may be more vulnerable to stress-precipitated relapse due to allostatic dysregulation of neural stress circuitry (Valdez & Koob 2004).

Like stress, thought suppression significantly decreased over the course of ten weeks of mindfulness training. In turn, decreases in thought suppression among MORE participants were significantly correlated with decreases in impaired alcohol response inhibition, raising the possibility that participants who improved their ability to regulate drinking urges may have done so via reductions in thought suppression.

In the context of alcohol dependence, thought suppression seems to enhance the conscious awareness of alcohol-related cognitions and affective reactions. MORE, with its emphasis on nonjudgmental, metacognitive awareness of present-moment experience, appeared to counter this deleterious cognitive strategy and therefore may have prevented post-suppression rebound effects from exacerbating negative affect and intrusive alcohol-related cognitions that can promote relapse.


In sum, the unwitting attempts of recovering alcohol dependent persons to suppress appetitive cognitive-emotional reactions towards alcohol may obscure these responses from consciousness only to perpetuate and intensify them within the cognitive unconscious. In the domain of unconscious mental life, automatic processes run smoothly and efficiently uninhibited by volitional control (Kihlstrom 1987). Hence, by shunting appetitive reactions into the unconscious, the alcohol dependent individual may increase the very appetitive response towards alcohol he or she is trying to suppress and exacerbate psychophysiological reactivity to alcohol cues. Mindfulness training may serve to undo this process, making unconscious responses conscious. Thus, practice of mindfulness may promote the recovery of alcohol dependent persons through: a) deautomatization of alcohol use action schema, resulting in diminished attentional bias towards subliminal alcohol cues and increased craving as a result of disrupted automaticity; and b) decreased thought suppression resulting in increased awareness of alcohol urges over time, increased HRV recovery from alcohol cue-exposure, and improved ability to inhibit appetitive responses.

Accordingly, mindfulness training may be a tractable means of promoting enduring behavior change. Although brief motivational interventions may be highly effective at impelling the desire towards sobriety, participants of such motivational enhancement therapies remain prone to eventual relapse; indeed, relapse is often a part of the recovery process. As such, interventions that consolidate short-term treatment gains into broader lifestyle change are of major significance to the addictions treatment field. During the gradual practice of mindfulness, one learns to work with negative emotions in a metacognitive context, resulting in nonreactivity to difficult mental contents and improved self-regulation in the face of stressors. The developmental process of cultivating and embedding mindfulness principles into all aspects of one’s life may solidify gains made in prior treatment and provide an effective, long-term approach to coping with stress-precipitated relapse.

Despite evidence suggesting that stress appraisal and attentional biases are key components of alcohol dependence, the form of addictions treatment most available to poor and marginalized persons, social support groups, does not target these pathogenic mechanisms directly. In contrast, practice of mindfulness may attenuate stress reactivity and thought suppression while disrupting addictive automaticity, resulting in increased awareness of craving and greater ability to cope with and recover from alcohol urges in stressful contexts. Hence, mindfulness training may hold promise as an alternative, targeted treatment for stress-precipitated alcohol dependence among vulnerable members of society.”

Equally mindfulness meditation may be used alongside other treatment regimes. For example, it can be used in a daily manner as part of step 11 in the 12 step program. It is also used as part of DBT, for example.

I think that there are ideas out there, is so-called different treatment regimes, which can simply compliment each other. Whatever works, works.

I personally meditate using both  Christian and Buddhist meditation techniques.

Sometimes appreciating the therapeutic strengths of different treatment philosophies and practice can augment one’s own main treatment and recovery program.


1.  Garland, E. L., Gaylord, S. A., Boettiger, C. A., & Howard, M. O. (2010). Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence: results of a randomized controlled pilot trial. Journal of psychoactive drugs, 42(2), 177-192.


The terror of “Locked In” Attention!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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



1. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry54(12), 1427-1436.




The Heart of Recovery

How is low HRV related to longer term recovering alcoholics?

We cited and use excerpts from a study (2) into short term and longer term (3) of up to six months which shows that alcoholics with years of recovery still have low HRV although it improves although this is dependent of severity of the alcoholism.

“It is known that chronic and heavy alcohol use has a toxic effect on the nervous system,[2] including effects on autonomic nervous system.[3] Specifically, heavy alcohol use can cause cardiac autonomic neuropathy,[4] which in turn, is associated with greater mortality.

Resting cardiac autonomic function reportedly favors energy conservation by way of parasympathetic dominance over sympathetic influence. Heart rate is characterized by beat-to-beat variability over a wide range, which has been reported to indicate vagal dominance and thereby parasympathetic dominance.[5]

In those with alcohol dependence, HRV is lower than in healthy individuals even after several days of abstinence.[13,14] This decrement may improve with abstinence for long periods of time.[15,16]

A study of 24-h ambulatory HRV found significantly reduced HRV in alcohol-dependent men with established vagal neuropathy and in some without.[17] Alcohol dependence has been shown to compromise vagal output measured before sleep onset, which correlates with loss of delta sleep and morning sleep impairments.[18]

Reduced HRV was found in alcohol-dependent patients with negative mood states and compulsive drinking.[19] Rechlin et al.,[20] reported reductions in HRV in patients with alcohol dependence, and this has been consistently reported in subsequent studies.[21,22]”


“Heart rate variability (HRV) was studied in 11 chronic alcoholic subjects, 1–30 days after the beginning of abstinence and again 5, 12 and 24 weeks later. Two patients could be re-examined after 19 and 22 months, respectively. In the follow-up study, the total patient group showed a statistically significant increase in HRV with prolonged abstinence of at least 6 months.

No recovery of efferent vagal function was found in 4 patients. It is suggested that the vagal neuropathy may improve in chronic alcoholics, but perhaps only in patients with a short to moderately long duration of drinking history (3)”.

Thus it seems thee is a partial recovery in HRV as recovery proceeds although there may be work required depending on severity of one’s alcoholism.

In our next blog on HRV we will cite and use excerpts from one of the best articles authored by Thayer which is the best explanation of how low HRV keeps an alcoholics attention “locked in” to stuff he/she would rather it didn’t get locked into such as alcohol-related cues.


1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

2. Ganesha, S., Thirthalli, J., Muralidharan, K., Benegal, V., & Gangadhar, B. N. (2013). Heart rate variability during sleep in detoxified alcohol-dependent males: A comparison with healthy controls. Indian journal of psychiatry, 55(2), 173.

3. Weise, F., Müller, D., Krell, D., Kielstein, V., & Koch, R. D. (1986). Heart rate variability in chronic alcoholics: a follow-up study. Drug and alcohol dependence, 17(4), 365-368.

Recovery is a Journey from the Head to the Heart (and back)!


So what does this low HRV mean for the recovering alcoholic?

I have explained this to show that HRV is directly connected to areas of the the brain implicated in stress and emotion regulation.

If, via recovery practices, we can still our beating heart, become serene as well as clean, it will have neuroplastic effects on our brain and the regulation of emotion and stress.

Equally if we meditate and alter the functioning of areas implicated in this study such as areas of the medial PFC and cingulate gyrus we improve our control over our heart. Ultimately if we can learn to relieve the inherent distress at the heart of addiction we can recovery function of not only the heart but also of areas in the brain which interact with the heart in producing heart rate variability.

So ultimately we need only to know how to quell a distressed heart via prayer, meditation, loving others.

If we can do so, we improve our emotion and stress regulation.

But do we need to do this if we have been in recovery long term?

Let me give you an example of allostasis in action.

In an allostatic system like addiction there is stress dysregulation coupled with reward dysfunction (I believe there is a pre-morbid allostasis in those addicts who have experienced abuse, trauma and insecure attachment also which means there is a stress and emotion dysregulation from an early age which leads to a heightened reward sensitivity which means we start to regulate negative emotions from an early age via impulsively  using or consuming stuff we really really like, or seem to like more than healthy people, to make ourselves feel better).

These adolescents at risk also have low HRV and the effects of alcohol have a pronounced effect on HRV.

This sets the chain of addiction in action from the start for many addicts.

So when we decide we want something this leads to a feeling of pathological wanting and then needing simply because we have altered reward systems as they are linked to our “out of kilter” stress systems .

Buying something in the store, if thwarted, soon becomes a life and death like struggle. Ever had that feeling?

I remember a 75 year old recovering person with 30 odd years of recovery  sharing in a meeting how she went to a store to get something, to find that something wasn’t there, so she was instructed to drive somewhere else to get that something, and when she got there they didn’t have it, so she had an argument with them and then with her husband in the car, then off to another store which did not have the something either, then back home on the internet, found a online store that stocked the something and ordered it.

It arrived the next day because she paid a lot of money for it to arrive the very next day! When it arrived she found that she had not only completely forgot about ordering the something but did not really want the something even. So off she sloped to apologise to her husband for being so emotionally abusive and immature over the something on her way to the Post Office to post back the something that she never really wanted in the first place!!?

This is also my head still, even after a few years of recovery. It is not as bad it was, by a long shot! It does, however, get distressed, I become impulsive and  want, need, that thing now!!! On occasion.

So I think this is one area recovery people always need to be aware of. Wanting stuff.

As it can lead to pathological wanting fairly quickly – then people get in the way of those things and we get angry, frustrated, distressed, our emotions overwhelm us or we are mean to our fellow human beings all because they are getting in the way of the thing I really really want.. NEED God damn it!…

We lose our emotional sobriety.

When we have either got it, regardless of the the human or emotional cost, we often find we do not want it or never really wanted it…that much….

Not compared to the cost of getting it!?

How do we solve this problem? We let go, we calm down, talk to someone, express our feelings, try to establish a transient homeostasis, let our stress systems subside and start again, trying to managing these chaotic brain systems.

Amends time.

If you are like that you have a low HRV and a stress/emotion regulation problem and probably always will.

But if can be manged and it can vastly improve. Then one day we learn that it is in living with our hearts forefront to our decisions and not our heads that brings lasting everyday happiness.

That is why in recovery we travel from our at times over zealous heads to our hearts. The wisdom and direction and basis of our decision making lives their not in our heads. It is not to say we do not use these wondrous instruments but we incorporate the help of our hearts in activating the reasoning of the brain.

Solve the heart issue, and the rest comes.


Neural structures associated with HRV

Over the past several years however a number of human neuroimaging studies have appeared in which researchers have explicitly examined the brain structures associated with HRV. In the present paper we provide a meta-analysis of eight published studies in which HRV has been related to functional brain activity using either PET or fMRI

The goal of this meta-analysis was to identify areas that were consistently associated with HRV.

In the overall analyses three regions show significant activations One region in the medial PFC (MPFC) is the right pregenual cingulate (BA 24/32).

Brodmann Cytoarchitectonics 24.pngBrodmann Cytoarchitectonics 32.png


Another MPFC region is the right subgenual cingulate (BA 25).

Brodmann Cytoarchitectonics 25.png

The third region is the left sublenticular extended amygdala/ventral striatum (SLEA). This region extends into the basolateral amygdalar complex, and also covers the superior amygdala (central nucleus) and extends into the ventral striatum.



More generally, the pgACC/rmPFC correlation with HRV in our meta-analysis suggests thatthis region is part, and the most reliably activated part in studies to date, of a descending “visceromotor” system that controls the autonomic nervous system and possibly other responses (neuroendocrine) based on emotional context.

The meta-analysis provides supportfor the idea that HRV may index the degree to which a mPFC-guided “core integration” system is integrated with the brainstem nuclei that directly regulate the heart. Thus these results support Claude Bernard’s idea that the vagus serves as a structural and functional link between the brain and the heart. We have proposed that this neural system essentially operates as a “super-system” that integrates the activity in perceptual, motor, interoceptive, and memory systems into gestalt representations of situations and likely adaptive responses. These findings suggest that HRV may index important organism functions associated with adaptability and health.”


1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

Journey from the Head to the Heart (and back)!

Part 1

Over this week leading up to my interview/podcast with sincerightnow

I want to look at the “neuroscience of alcoholism and addiction from another angle. I want to look at the evident difficulties seen in alcoholics in terms of impaired self and emotion regulation by looking at the relationship of the heart to the brain.

Some may find this a more clear, easier way to understand what is impaired in terms of brain functioning in alcoholics. I know I do and looking at the role of the heart in alcoholism has helped me understand the issues more clearly. I hope it does for you too.

I will seek to explain how the emotional, stress and thus self dysregulation seen in alcoholics and addicts is indexed or can be seen clearly in terms of a reduced heart rate variability  compared to normal healthy individuals.

I will explain as we go, how low HRV is linked to this dysregulation gives rise to a stress and emotion reactivity and an impulsivity seen commonly in alcoholics in particular.

This low HRV has a interactive effect in the emotion regulation  parts of the brain also with one effecting the other. So in terms of say reducing distress, stress and thus craving, for example, we could suggest instead use measures to improve low HRV such as mediation and so on. If we get the heart under more control, the neurotransmission of the brain and stress chemicals too seem also to be affected.

It certainly ties in with treatment regimes which advocate strategies of letting go of distress and maintaining balance and serenity.

Personally I find it fascinating how the heart can affect the workings of the brain.

Before we look at the concept of heart rate variability in relation to alcoholism we need to first to look at the interaction between the head and the heart.

We cite and use excerpts from a review (1) by Julian Thayer, one of the leading experts on the subject of heart rate variability (HRV) and it’s relationship to impaired self and emotion regulation.

“The intimate connection between the brain and the heart was enunciated by Claude Bernard over 150 years ago.

Heart rate variability may provide an index of how strongly ‘top–down’ appraisals, mediated by cortical-subcortical pathways, shape brainstem activity and autonomic responses in the body.

Thus, HRV may serve as a proxy for ‘vertical integration’ of the brain mechanisms that guide flexible control over behavior.

We have proposed that a core set of neural structures provides an organism with the ability to integrate signals from inside and outside the body and adaptively regulate cognition,perception, action, and physiology.

This system essentially operates as a “super-system” that integrates the activity in perceptual, motor, interoceptive, and memory systems into gestalt representations of situations and likely adaptive responses. Thus, it is undoubtedly extremely complex. However, it is still possible that physiological measures exist that can serve as indices ofthe degree to which this system provides flexible, adaptive regulation of its component systems. In a number of papers (Thayer and Brosschot, 2005; Thayer and Lane, 2000, 2009), we have proposed that heart rate variability (HRV) may provide just such an index.

However if component systems are become unbalanced, and a particular process can come to dominate the system’s behavior, rendering it unresponsive to the normal range of inputs. In the context of physiological regulation, and regulation of the heart specifically, a balanced system is healthy, because the system can respond to physical and environmental demands (Thayer and Sternberg, 2006). A system that is “locked in” to a particular pattern is dysregulated. This is why the heart rate of a healthy heart oscillates spontaneously (i.e., shows high HRV), whereas a diseased heart shows almost no variability under certain conditions. A critical idea is that HRV may be more than just an index of healthy heart function, and may in fact provide an index of the degree to which the brain’s “integrative” system for adaptive regulation provides flexible control over the periphery. Thus, HRV may serve as an easily measured output of this neural network that may provide valuable information about the capacity of the organism to effectively function in a complex environment.


Hear Rate Variability

Like many organs in the body, the heart is dually innervated. Although a wide range of physiologic factors determine cardiac functions such as heart rate (HR), the autonomic nervous system (ANS) is the most prominent with Although a wide range of physiologic factors determine cardiac functions such as heart rate (HR), the autonomic nervous system (ANS) is the most prominentwith  both cardiac vagal (the primary parasympathetic nerve) and sympathetic inputs.



The heart is under tonic inhibitory control by parasympathetic influences. Thus, resting cardiac autonomic balance favors energy conservation by way of parasympathetic dominance over sympathetic influences. In addition, the HR time series is characterized by beat-to-beat variability over a wide range, which also implicates vagal dominance as the sympathetic influence on the heart is too slow to produce beat to beat changes.

Low heart rate variability (HRV) is associated with increased risk of all-cause mortality, and low HRV has been proposed as a marker for disease (Thayer and Lane, 2007; Thayer et al., 2010b). The basic data for the calculation of all the measures of HRV is the sequence of time intervals between heart beats. This interbeat interval time series is used to calculate the variability in the timing of the heart beat. As mentioned earlier the heart is dually innervated by the autonomic nervous system such that relative increases in sympathetic activity are associated with heart rate increases and relative increases in parasympathetic activity are associated with heart rate decreases.

Thus relative sympathetic increases cause the time between heart beats (the interbeat interval) to become shorter and relative parasympathetic increases cause the interbeat interval to become longer.

The differential effects of the ANS on…s the timing of the heart beats, are due to the differential effects of the neurotransmitters for the sympathetic (norepinephrine) and parasympathetic (acetylcholine) nervous systems. The sympathetic effects are slow, on the time scale of seconds, whereas the parasympathetic effects are fast, on the time scale of milliseconds. Therefore the parasympathetic influences are the only ones capable of producing rapid changes in the beat to beat timing of the heart.

In summary, the heart and the brain are connected bidirectionally. Efferent outflow from the brain affects the heart and afferent outflow from the heart affects the brain. Importantly, the vagus is an integral part of this heart–brain system and vagally mediated HRV appears to be capable of providing valuable information about the functioning of this system.


HRV and emotional regulation In addition to being linked to vmPFC and amygdala modulation, emotion regulation is linked to HRV (Appelhans and Luecken, 2006; Thayer and Brosschot, 2005). Individuals with greater emotion regulation ability have been shown to have greater levels of restingHRV(Appelhans andLuecken,2006; Thayer andLane,2009). In addition, during successful performance on emotion regulation tasks HRV appears to be increased (Butler et al., 2006; Ingjaldsson et al., 2003; Smith et al., 2011).

We have investigated the role of HRV in emotional regulation attwo differentlevels of analysis. One level is at the trait or tonic level where individual differences in resting HRV have been associated with differences in emotional regulation. We have shown that individuals with higher levels of resting HRV, compared to those with lower resting levels, produce context appropriate emotional responses as indexed by emotion-modulated startle responses, fear-potentiated startle responses, and phasic heart rate responses in addition to behavioral and self-reported emotional responses (Melzig et al., 2009; Ruiz-Padial et al., 2003; Thayer and Brosschot, 2005). In addition, we have recently shown that individuals with low resting HRV show delayed recovery from psychological stressors of cardiovascular, endocrine, and immune responses compared to those with higher levels of resting HRV (Weber et al., 2010). Thus, individuals with higher resting levels of HRV appear more able to produce context appropriate responses including appropriate recovery after the stressor has ended.

Another level of analysis is at the state or phasic level where HRV values increase during the successful regulation of emotion during emotion regulation tasks. Thus, it has been shown that phasic increases in HRV in response to situations that require emotional regulation facilitate effective emotional regulation. In an early study, we showed that HRV increased in recovering alcoholics in response to alcohol cues but only if they later reported an increased ability to resist a drink. Those recovering alcoholics that later reported an urge to drink did not exhibit increased HRV during the alcohol cues (Ingjaldsson et al., 2003). A recent replication and extension of this work reported increased HRV during the successful regulation of emotion by either reappraisal or suppression (Butler et al., 2006). We have recently shown that the increase in HRV associated with emotional regulation is accompanied by concomitant cerebral blood flow changes in areas identified as being important in emotional regulation and inhibitory processes (Lane et al., 2009).

, the amygdala, which has outputs to autonomic, endocrine, and other physiological regulation systems, and becomes active during threat and uncertainty, is under tonic inhibitory control via GABAergic mediated projections from the prefrontal cortex (Davidson, 2000; Thayer, 2006).

. Thayer and Lane (2000) suggested that a common reciprocal inhibitory cortico-subcortical neural circuit serves as the structural link between psychological processes like emotion and cognition, and health-related physiological processes, and that this circuit can be indexed with HRV. Thus, because of these reciprocally interconnected neural structures that allow prefrontal cortex to exert an inhibitory influence on sub-cortical structures, the organism is able to respond to demands from the environment, and organize their behavior effectively. In the next section we briefly review the evidence for the relationship of HRV to this network of neural structures and further specify the prefrontal regions involved in the inhibitory control of the heart.




1. Thayer, J. F., Åhs, F., Fredrikson, M., Sollers, J. J., & Wager, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: implications for heart rate variability as a marker of stress and health. Neuroscience & Biobehavioral Reviews, 36(2), 747-756.













Insecure attachment affects emotion regulation in alcoholics?

I have blogged recently about how insecure attachment is linked to various addictive behaviours.

What is important is to establish a mechanism by which insecure attachment contributes to later addictive disorders. It may not be enough to say attachment and addiction are linked but that they are linked via a pathomechanism of some sort.

I have argued many times before that I believe this pathomechanism, the mechanism by which a pathological condition occurs, or the mechanism that  drives a disease state (or disorder) is emotion processing and regulation deficits.

We look here (1) at a study that demonstrates how insecure attachment correlates in alcoholics with difficulties in emotion processing and regulation difficulties. I believe this is how addiction is driven to it’s endpoint of chronic, compulsive behaviour, although this study is only a correlational study and makes no such claims about causation.

Attachment theory has been conceptualised as an affect regulation theory, proposing that attachment is associated with the expression and recognition of emotions as well as interpersonal functioning… the objective of the present study was to investigate potential associations between attachment, Negative Mood Regulation (NMR) expectancies, fear of intimacy and self-differentiation…(with)  findings support broad attachment theory suggesting that attachment is associated with and predicts affect regulation abilities, difficulties with intimacy and intrapersonal as well as interpersonal functioning in a sample of substance use disorder inpatients.

Attachment is associated with the expression and regulation of emotion. Early attachment theory postulates that early bonding
with a significant caregiver is essential for the development of internal working models for communication, regulation of emotions and interpersonal behaviour.

These early attachment experiences are associated with adult attachment styles. Adult attachment styles are relatively stable and influence attitudes, emotions, affect regulation and behavioural strategies in relationships…Empirical evidence has indicated associations between insecure attachment, fear of intimacy and
emotion regulation difficulties  and between secure attachment
and a higher capacity for intimacy, emotional awareness and empathy.

Substance abuse has been proposed to be a consequence of emotion regulation difficulties with individuals using alcohol/drugs to avoid
intimacy or rejection, to ease pain, anger and ambivalence and possibly establish a “secure base”.

Negative mood regulation (NMR) expectancies are beliefs regarding a person’s ability to terminate or alleviate a negative mood state.

High NMR presumably reflects the ability to cope successfully with bad moods, whereas having low NMR may lead to less efficacious or maladaptive ways of coping… high NMR may be associated with secure attachment, as securely attached individuals tend to seek comfort from others when emotionally upset, and utilise constructive coping mechanisms to decrease the intensity of distress.

By contrast, low NMR may potentially be associated with anxious attachment as well as substance abuse...insecure attachment is a fearful attachment style characterised by a fear of intimacy and rejection, high emotional reactivity and a self-belief associated with being deserving of rejection. Some have argued that fear of intimacy (FIS) is associated with mental health issues and substance use problems…FIS research to date has largely reported significant associations with loneliness, lack of self-disclosure, low social interaction and low relationship quality.

Differentiation of self is defined as the degree to which an individual is able to balance emotional and intellectual functioning, intimacy and autonomy in relationships…Individuals with lower
self-differentiation experience higher levels of chronic anxiety, emotion regulation difficulties, mood disturbances and substance abuse.

In addition, previous studies have reported higher levels of mood regulation and interpersonal difficulties in substance abusers compared to controls…(As) attachment has been hypothesised to be associated with relationship functioning and mood regulation (and)  addiction has been proposed to be an attachment disorder,  potential relationships of attachment with mood regulation and interpersonal functioning in substance abusers may
potentially inform the development of future treatment approaches.

The results (of this study) indicated a significant negative association between anxious attachment and NMR…suggesting that anxious attachment may be associated with lower abilities to regulate one’s negative moods. This is in accordance with other research evidence suggesting that insecurely attached individuals tend to show poor affect regulation.

The present investigation also found that attachment was a strong predictor of FIS (and)  the present results suggest that adult
attachment is related to difficulties in intimacy and interpersonal functioning, in accordance with previous evidence that reported a significant association between insecure attachment and relationship problems as well as lower levels of trust, interdependence and commitment.

The present investigation also found that anxious attachment significantly predicted emotional reactivity (ER).

These data support the predictive power of anxious attachment in relation to being more emotionally reactive, having difficulties with emotion regulation and maladjustment in those with substance dependence…The predictive utility of attachment was also related to Emotional cut-off (EC)…This is in line with previous research suggesting a link between attachment and EC  in those with substance abuse and implies that attachment style is related to traits of emotional aloofness, anxiety, isolation from others and exaggerated independence…EC may be associated with, or a consequence of alexithymia, a personality trait associated with difficulties in identifying and describing feelings.”

The above sounds so familiar, doesn’t it? Sounds like most newcomers to recovery that I have ever come cross, including me.


1.  Thorberg, F. A., & Lyvers, M. (2009). Attachment in relation to affect regulation and interpersonal functioning among substance use disorder in patients.Addiction Research & Theory, 18(4), 464-478.