Finally Found What We Were Looking For

Quenching that Spiritual Thirst

I have been keeping up  my regime of getting more spiritually fit – went to mass and then a meeting.

I have also been doing a lot of walking too (approx 5 miles a day).

Although I still blog on the neuropsychology of addiction on my other blog (kinda alcoholic having two blogs isn’t it?) http://insidethealcoholicbrain.com/ my heart and soul is moving noticeably back into the world of recovery and doing recovery.

My head has been learning what my heart knows already.

Not just turning up at a meeting and sharing my experience and insights but also doing low level service, like always helping clear up after the meeting, stacking chairs, moving tables etc.

I have also enjoyed talking to newcomers. It has been fascinating meeting people where they are at.

Rather than using my memory banks to relate my stories of treatment and recovery,  I am more interested in their own spiritual journeys of self discovery.  I kinda feel excited for them.

It is always spiritually nourishing to see people suddenly get it, to see the light of recognition and acceptance of their condition start shining a new light in their eyes. The beginnings of psychic change and a spiritual awakening about their condition.

I go to chapel  but rarely see this type of transformation. Perhaps the people at mass aren’t as spiritually ill as us? I am not so sure sometimes.

I shared this with an earthling/normie who had some experience of 12 step groups and she agreed most enthusiastically that the conversions one sees in 12 step groups appears more profound than any she experienced in chapel.

It makes one think this – how is is that a hopeless drunk can suddenly be so dramatically altered in his or her views of the world and those in it. How come they can come to accept a higher power in their lives so readily? Almost as if they had some strange disposition towards this?

Is this part of the gift of desperation? Is it partly an acceptance of seeing it work in others and this encourages one to explore this themselves?

Is it because there is close link about being humiliated by alcohol and the necessary ego deflation which leads to humility (for me humility is tied up with accepting one needs help and then asking for and receiving it)?

When i came to AA I was determined not to do the God thing but I intuitively understood the spiritual thing.

I had been a practicing Buddhist on and off over a decade or more and firmly believed that all suffering comes from an attachment to the self. I still do.

Hadn’t I already been looking for a spiritual solution to my problems?

 

 

Both my parents were very religious and both had issues with alcohol (my father before I was born) and drugs (Valium in my mothers case). In fact my parish priest was an alcoholic and my father would have to go the the parish house at least half an hour prior to mass to make sure he was sober enough to take mass. A beautiful man he was too, our local priest but an active alcoholic.

Was I born into this world with a spiritual thirst, a thirst for communion with the infinite, something beyond the self, with the divine in order to escape the often emotionally painful limitations of the self?

Has it always been necessary for me, spirituality? Does in balance my inherent lackings?

Before I went to mass I meditated for half an hour. I used this Christian meditation where I simply lie in a corpse position on my back and wait or God’s Grace. Sometimes I utter the words “Come Holy Spirit Come” and give myself wholly to His Grace.

Then I have this creeping feeling of peace, of stillness, of quiet.

I have some of the thoughts I normally have but they do not effect me, they are no longer exerting any distress and I no longer react to them. They are no longer propelling me out of bed and into some course of action.

They are my thoughts devoid of anxiety, devoid of emotional pain.  But they are still mine but cwtched in the comforting embrace of God.

To be an addict about it – it is like an analgesic, a pain killer in a sense. Like an opiate but without the disappearance from reality, instead remaining still but present in the now, in this moment.

The best way I can help explain further is in relation to the video below where Thomas Merton describes contemplation and mystical union with God.

This helped me a great deal this video because when talking of God we have to be careful we are not creating a self construction of God which leaves us still in the finite parameters of self and self delusion.

It is beyond self but it is a realm in which the self communes with that beyond oneself. Thomas Merton explains it better than I ever could!

It is the sense of the infinite, the escape from the attached self, the transcendence that I have always wanted, craved and finally compulsively sought .

Why did I not find it fully before? Why, well I think this is because I had always had this other way of finding transcendence and that was in a bottle or in a drug or in a behaviour.

I could not fully find this divine transcendence until I saw the lies of this chemically created transcendence.

It had always been getting in the way of what I really need, a full God consciousness, full transcendence from self.

After the meeting I stopped and talked with two elderly woman and then walked them up the street to where they were going. We laughing and carrying on, gently making fun of each other, stopping to talk and go on, then stop again and go on, with silly talk and laughter.

We stopped and staggered our talkative ways on the hill to Main Street. Arm in arm with foolish fun. To the outsider we must have looked like we were acting like three drunks would, talking, and excessively gesturing, caught up in waffly exuberance. Slightly intoxicated by our merriment.

I remember thinking this is similar to going out on the town with friends, who mainly were alcoholics too and are mainly now dead.

We could have looked like three drunks who had finally  found what they were looking for!

Drink was never the answer, it got in way of the answer but also kept some of us from killing ourselves while we waited for this answer, His Mercy.

 

God blesses AA!

 

Filling that “Hole in the Soul”

When I first  arrived in AA I was told by a big scary looking man that in AA you will get better.

That “we will help you by loving you back to health”.

I was quite alarmed by this situation to be honest “loved back to health”? Was this guy some relic from the hippy era?

What he said, was very threatening to me. It suggested unconditional love, a concept that I was only partially familiar with.

I had always knew my father loved my unconditionally but this was less the case with my mother. I knew she loved me in her vague, through a  distant Valium haze but part of me was always reaching out, crying out for more. More love.

I found that love in liquid form in alcohol. Or so I felt. Alcohol was constant. It always delivered without fail, transported me to the person I would much rather be. Allowed me to escape the person I did not want to be.

I now accept my mother suffered from addiction just like me and I have immense compassion for her because of that, she did the best she could under the circumstances. I forgive her completely and love her completely.

She was not a bad person she as an ill person just like me.

Did this relationship with my primary care giver have any effect on my teenage drinking and later alcoholism?

Like many alcoholics I have spoken to over the years I too seemed to suffer from the  “hole in the soul” they spoke of.

That not feeling whole, like something in you, some part of you was missing.

Having a curious mind, I always wondered what it could be? It must be something that can be discovered? I wasn’t happy to leave it was a vague spiritual condition.

It felt too emotional just to be a spiritual thing, although it is also that.

It felt like I was lacking in something, something in my make up was not there or in diluted measure?

Later I found out that this relationship with my mother was called an insecure attachment and that lots of people in recovery had this insecure attachment with their mothers or whoever reared them.

This insecure attachment they said often resulted in novelty seeking and hunting out some “secure attachment” elsewhere, in a bottle, syringe, sex, a poker machine, food or other addictive behaviours.

It is lonely recently that I found there is a brain chemical linked to this insecure attachment called oxytocin, the “love chemical” which effects all the neurochemical said to be involved in addiction.

Oxytocin is badly affected by the stress reaction to insecure attachment, abuse trauma and a tough upbringing. The oxytocin is then reduced which reduces the other chemicals too and we search for these at the bottom of a glass.

Unfortunately alcohol seems to give us cocktail of these chemicals in liquid form. But never enough.

For a while anyway, it gives us the illusion of attachment, of that fleeting feeling of being part, of being loved.

Through the years all these chemicals start running dry and the drink stops working.

We are then left with the problems we had before we put a glass to our mouths.

So when the drink stopped working and I had to go to AA – not one wants to go  there, let’s face it, it’s because we have to!

So the big scary guy may have been right all along. I have found that he is right over the years of attending AA.

I have found a new, surrogate family  in AA, a “learnt attachment” within the fellowship of others in the same boat as me, who have felt the same as me. I have found this attachment to others, by being looked after and trying to help others – my oxytocin, the “love chemical” the “cuddle chemical” has gone up dramatically while my stress has plummeted as I have bonded with others in recovery.

This connectedness is my spiritual solution to a neurobiological problem.

I now feel part of for the first time, I have filled the hole in the soul with love given and received.

Who Wants to be an Alcoholic?

The social stigma of being an alcoholic prevents many from coming into recovery and treating their illness. And it is an illness but it takes time to realise that – a physiological, psychological, emotional, cognitive, behavioural and spiritual disease. It is as profound an illness as one can have.

It is the only illness that actively tells you that you do not have it!

How cunning, baffling and powerful is that!?  

In fact stigma, particular prevalent in the UK as compared to the US, helps kill alcoholics.

We all have ideas of tramp on park benches supping on bottles of alcohol when we think of alcoholics.

I know I did. When I went to my first meeting I thought I would be greeted by park tramps with strings holding their trousers up with food encrusted beards, no teeth and hygiene problems.

I wasn’t greeted by anyone like this.

I was greeted by a teacher, a lawyer, a counsellor, a business man, a builder, a nurse, an actress, among others.  Alcoholism effects every area of life, no strata of life is immune, there are recovering alcoholics everywhere.  The second man to have stepped on the moon is in recovery for alcoholism!

These shiny AA people were not drinking and some had not drank for decades!

Imagine not drinking for ten years and more? I could not imagine ten minutes…but now I am coming up to my tenth birthday in AA.

 

“Most of us have been unwilling to admit we were real alcoholics. No person likes to think he is bodily and mentally different from his fellows” (1)

Neuroscience has demonstrated repeatedly how the brain is taken over by the actions of alcohol and other substances which leave the brain severely restricted in it’s choice of behaviours. Self will has become so compromised we barely have any!?

We become so comprised in our own ability to make decisions that we are often “without mental defence against” drinking.

Alcohol via the alterations in stress and reward (survival) systems in the brain means our illness has literally taken over our brain and calls the shots, does the thinking which leads to the drinking.

We have a thinking disease as well as drinking one by the time we get into recovery.

It is the thinking of this illness, which we mistake for our own, quite understandably, as these thoughts are happening in our own head, that tells us we do not have an alcoholic problem, we do not need to go to an AA meeting, or when we have gone, that we do not need to stay, that we are different to the people at the meeting – that they need this recovery thing not me. I can work this out myself.

Why does it do this?

Why is it constantly chittering away between our ears. It has to be us, surely? Our thoughts can’t have been taken over like some 1960s episode of Star Trek where Captain Kirk and crew are struck down by some thought virus??

If you are new to recovery don’t bend your head over this stuff!

All you have to do is twofold. Get to a meeting and see if your experience of drinking tallies with those there and two, watch out for that motivational voice of alcoholism trying to get you far away from these people.

This is my test to see if you are alcoholic.

This voice of the illness is similar to the voice of OCD and other anxiety disorders which talk to us in thoughts which are contrary to our well being and health. Why?

Because our survival networks in the brain have gone so haywire that these conditions think they are helping us survive by suggesting certain actions which we previously used to reduce distress, i.e.compulsive behaviours, but which take us increasingly into even greater emotional distress and unhealthy behaviours.

They are like an Olympic coach training us to get chronically unwell.

They persist because they have ingrained in our brains unfortunately, possible forever. They are the torturous whispers of our neural ghosts!

They refuse to die but in time these voices become more manageable, the volume on them can be turned down or ignored altogether.

Turning down the distress signal that feeds them is at the key.

You are not alone – “Every natural instinct cries out against the idea of personal  powerlessness.” (2)

This powerlessness led me to surrendering. Paradoxically to win this war we must first surrender.

Surrendering to the idea that I may, possibly, be an alcoholic.

Acceptance of this possibility is the first step.

 

References

 

  1.  Alcoholics Anonymous. (2001). Alcoholics Anonymous, 4th Edition. New York: A.A. World Services.
  2. Twelve steps and twelve traditions. (1989). New York, NY: Alcoholics Anonymous World Services.

 

You are Not Alone!

In the final months of my active alcoholism I was living in the attic room of my house.

I drank about 6 bottles of cheap Spanish wine plus a dozen cans of strong German beer every day.

The alcohol had little effect on me by this stage. I only drank to dampen the delirium tremens, the violent shakes. I often could not control my hand enough to get alcohol into my mouth, holding my wrist steady with my other hand to raise the drink to my mouth.

Usually  cracking the bottle or tin can against my teeth.

I was no longer getting drunk anymore.

You know you are fully addicted to alcohol when it does nothing intoxicating any more.

I slept in 5-10 minute fits and busts. I did not eat for months. The television told me to kill myself and voices not belonging to me talked insistently in my head.

Alcohol-related Psychosis it is called.

No one told me this would happen when I bought my first alcoholic drink when I was fourteen years old. There was no health or warning label saying “Could lead to Psychosis and Premature Death!”

Maybe there should be.  Or at least alcohol can be addictive for some.

Anyway there is more to alcoholism than alcohol.

In the depths of this alcohol induced madness, I rarely saw my wife, who could not bring herself to look at me and what I had become.

If I could have got it together I might have killed myself.

But I couldn’t get it together. Psychosis is all involving, doesn’t leave much time for planning anything.

 

 

So I staggered on. When I say staggered, I could not actually walk more than a few yards or climb more than a few stairs.

By  the time I reached my first AA meeting

1. the alcohol had stopped “working”.

2. I had surrendered.

Regardless of these two factors, I could not admit I was alcoholic. My pride and it’s best friend shame were still talking away to me.

I was willing to admit I was addicted to alcohol and that I was about to die from it.

But alcoholic?

We often wonder why some people don’t accept their alcoholism?

How did I start my journey to acceptance?

My wife came to my first meeting of AA, she practically carried me in!

The Chair of the meeting was a person I had drank with before – I though how come he is here?

I spilled more drink than he ever drank?

Then it dawned on me that maybe I should have come here before?

Especially when he shared that he had been trying to get sober and recovered for ten years!?

I then listened to the other alcoholics sharing their stories.

The stories mentioned the progression of the alcoholism, which I obviously identified with.

They also mentioned how they, even now in recovery, struggled with their emotions and anxieties, how they found living life difficult.

They talked about issues which had bedevilled them and me since childhood, this  spiritual malady they talked of was like the emotional disease I had  suffered from all my life, whether it was depression, panic attacks, anxiety disorders, PTSD, etc.

They had used alcohol to self medicate these conditions, especially as alcohol for them had felt like an elixir for them as it had for me.  We all had all dealt with our negative emotions since adolescence in the same way.

Now a new way had to be found.

When we left the meeting my wife had a psychic change similar to the one I had.

She said these people are just like you. They can help you, I can’t.

A week before I had heard a voice in my heart, through the psychosis, saying  to go down stairs to my wife and ask her for help. I asked her for help in that round about alcoholic way of “do you think I look a bit jaundice (I actually looked like Homer Simpson with a heavy sun tan!)?

The help I asked for was not to come directly from my wife but she led me to where I could get it. In a room, full of people just like me, suffering the same illness as me.

I will be forever eternally grateful for it being there for me. For them being there.

We will be there for you too!

Self Diagnosing Alcoholism

For those reading who feel they may a problem with alcoholism I will attempt to help you self diagnose.

I personally came into recovery via AA after my local doctor/GP, stated quite unequivocally that he thought I was an alcoholic. I was with my wife at the time.  The scales fell from our respective eyes.

Oh that’s it!? It wasn’t my troubled childhood, the premature death of my parents, my various difficulties with anxiety, depression, panic attacks, etc etc. It was because I was an alcoholic!

I have no doubt that the above factors contributed to the severity of my alcoholism but the other psychiatric issues I now consider to have been substance induced disorders which have either dissipated in recovery or have been treated in some way by a 12 step recovery?

Regardless of GP’s diagnosis of alcoholism I still need to self diagnosis.  I could not recover from alcoholism based on someone else’s diagnosis, however helpful. I had to identify myself as an alcoholic. Acceptance of this condition was the first step in recovery for me and countless others.

In the early days acceptance is based on acceptance of a destructive relationship with alcohol.

How do we define this relationship, this alcoholism?

There are various definitions of alcoholism mainly centring on  continued use of alcohol despite negative consequences. The Big Book of Alcoholics Anonymmous (1) simply states  “If, when you honestly want to, you find you cannot quit entirely, or if when drinking, you have little control over the amount you take, you are probably alcoholic.  “.

This useful useful article (2) discusses the “loss of control over drinking” concept, which academic studies have failed to prove or disprove in laboratory settings.

I believe this loss of control can occur spontaneously or over several drinking episodes. It is not an all or nothing phenomenon like the “allergy” concept of the Doctor’s Opinion in the Big Book. It is variable.

The return to uncontrolled drinking can take one drinking session for some or a number of drinking sessions for others.

“The loss-of-control phenomenon is the essence of any addiction and certainly of AD.

This refers to the inability of the AD person to predict with any degree of certainty how much he or she will imbibe from one drinking episode to the next.

Clinically, once the drinking episode starts, the AD person will be unable to stop in the middle of the episode without a very great struggle. Useful questions at interview include asking 1) whether patients feel compelled to continue drinking or find it very hard to stop drinking; 2) once they start, whether they find themselves drinking more than they wanted to or had planned to; and 3) whether they make rules to attempt to control their drinking through external means.

It is important to distinguish the loss-of-control phenomenon from craving. The former has to do with the inability to stop drinking once started.

The loss-of-control phenomenon occurs within a drinking episode. Forms of craving occur between drinking episodes. The loss-of-control phenomenon continues to be a scientific puzzle.

Despite ongoing research inquiry over many years, neuroscience has yet to define the CNS changes underlying the loss-of-control phenomenon that characterizes dependence.

Clinically, however, longitudinal studies of abstinence make it clear that once the control of drinking behavior departs, it does not return in most cases (3).

It cannot be relearned or reconstituted. In this sense, a diagnosis of dependence signals a permanent condition—including a permanent risk of uncontrolled drinking. “

 

 

  1. Alcoholics Anonymous. (2001). Alcoholics Anonymous, 4th Edition. New York: A.A. World Services.
  2. Beresford, T. P. (2007). What is addiction, what is alcoholism?. Liver Transplantation13(S2), S55-S58.
  3. Vaillant GE. The Natural History of Alcoholism, Revisited. Cambridge, MA: Harvard University Press; 1995.

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.

 

References

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

 

 

 

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

Part 1

Over this week leading up to my interview/podcast with sincerightnow http://www.sincerightnow.com/upcoming/ http://www.sincerightnow.com/pdcst/

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.

 

TBC

References

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.