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!

The Power of Identification!!

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

Or rather the first step can be simple.

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

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

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

Alcoholism increasingly takes away choice.

It takes over your self will.

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

Alcoholism takes over these networks, progressively, over time.

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

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

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

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

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

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

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

Can you see it in your life?

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

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

I did also relate to other things these people shared.

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

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

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

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

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

All of this was the case with me too.

I identified with all this.

I identified too with their solution.

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

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

There is a solution.

We do recover!

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.

 

 

 

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

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

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

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

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

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

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

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

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

 

impulse control.preview

“Abstract

Background

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

Results

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

Conclusions

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

Introduction

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

Predictors of Mortality Risk among Individuals with Alcohol Use Disorders

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

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

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

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

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

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

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

Discussion

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

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

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

Moderation of the Impulsivity-Mortality Link via the Social Context

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

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

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

References

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

Alcoholics Anonymous and Reduced Impulsivity: A Novel Mechanism of Change

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120px-Orbital_gyrus_animation_small2

 

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

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

128px-Amyg

 

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

 

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

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

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

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

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

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

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

The trouble it has caused is quite staggeringly really?

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

“Abstract

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

Among individuals with alcohol use disorders (AUD), Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [1, 2]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [3]. To our knowledge, however, there have been no efforts to examine links between AA and reductions in impulsivity-a dimension of personality marked by deficits in self-control and self-regulation, and tendencies to take risks and respond to stimuli with minimal forethought.

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

Impulsivity and related traits of disinhibition are core risk factors for AUD [5, 6]. In cross-sectional research, impulsivity is typically higher among individuals in AUD treatment than among those in the general population [7] and, in prospective studies, impulse control deficits tend to predate the onset of drinking problems [811]

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

Substance use-focused mutual-help groups may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [26]. Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations.

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

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

References

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

Why Alcoholics Anonymous Works

A journalistic piece entitled,  “The Irrationality of Alcoholics Anonymous “, written by  Gabrielle Glaser, also harshly criticizes Alcoholics Anonymous. AA and similar 12-step programs.

I cite a blog on her criticisms here (1)

Why Alcoholics Anonymous Works

“Glaser’s central claim is that there’s no rigorous scientific evidence that AA and other 12-step programs work.

First, she writes that “Unlike Alcoholics Anonymous, [other methods for treating alcohol dependence] are based on modern science and have been proved, in randomized, controlled studies, to work.” In other words, “modern science” hasn’t shown AA to work.”

Glaser appears to lessen her argument by suggesting that AA is difficult to study (so how can she be so sure it is not effective then?).

” Alcoholics Anonymous is famously difficult to study. By necessity, it keeps no records of who attends meetings; members come and go and are, of course, anonymous. No conclusive data exist on how well it works.”

Equally there, in her world view, would also be no conclusive data to suggest if doesn’t work? So why make bold claims either way?

” In 2006, the Cochrane Collaboration, a health-care research group, reviewed studies going back to the 1960s and found that “no experimental studies unequivocally demonstrated the effectiveness of AA or [12-step] approaches for reducing alcohol dependence or problems.”

According to (1), Glaser is simply ignoring a decade’s worth of science, not only here but throughout the piece.

“No, that’s not true,” said Dr. John Kelly, a clinical psychologist and addiction specialist at Massachusetts General Hospital and Harvard Medical School. “There’s quite a bit of evidence now, actually, that’s shown that AA works.”

Kelly, alongside Dr. Marica Ferri and Dr. Keith Humphreys of Stanford, is currently at work updating the Cochrane Collaboration guidelines (he said they expect to publish their results in August).

” Kelly said that in recent years, researchers have begun ramping up rigorous research on what are known as “12-step facilitation” (TSF) programs, which are “clinical interventions designed to link people with AA.”

Dr. Lee Ann Kaskutas, a senior scientist at the Alcohol Research Group who has conducted TSF studies, suggest that TSF outperforms many alternatives.

“They show about a 10 to 20 percent advantage over more standard treatment like cognitive behavioral therapy in terms of days abstinent, and typically also what we find is that when people are engaged in a 12-step-oriented treatment and go to AA, they have about 30 percent to 50 percent higher rates of continuous abstinence,” said Kelly.”

The original Cochrane paper that Glaser cites came out before the latest round of studies did, so that research wasn’t factored into the conclusion that there’s a lack of evidence for AA’s efficacy. In a followup email, Kelly said he expects the next round of recommendations to be significantly different:

Although we cannot as yet say definitively what the final results will bring in the updated Cochrane Review, as it is still in progress, we are seeing positive results in favor of Twelve-Step Facilitation treatments that have emerged from the numerous NIH-sponsored randomized clinical trials completed since the original review published in 2006. We can confirm that TSF is an empirically-supported treatment, showing clinical efficacy, and is likely to result also in lowered health care costs relative to alternative treatments that do not link patients with these freely available recovery peer support services. Another emerging finding is that a central reason why TSF shows benefit is because it helps patients become actively involved with groups like AA and NA, which in turn, have been shown to enhance addiction recovery coping skills, confidence, and motivation, similar to professional interventions, but AA and NA are able to do this in the communities in which people live for free, and over the long-term.

In other words, the most comprehensive piece of research Glaser is using to support her argument will, once it takes into account the latest findings, likely reverse itself.”

In other words, it will also help contradict Glaser’s arguments.

“In an email and phone call, Glaser said that TSF programs are not the same thing as AA and the two can’t be compared. But this argument doesn’t quite hold up: For one thing, the Cochrane report she herself cites in her piece relied in part on a review of TSF studies, so it doesn’t make sense for TSF studies to be acceptable to her when they support her argument and unacceptable when they don’t.

For another, Kelly, Katsukas, and Humphreys, while acknowledging that TSF programs and AA are not exactly the same thing, all said that the available evidence suggests that it’s the 12-step programs themselves that are likely the primary cause of the effects being observed (the National Institutes of Health, given the many studies into TSF programs it has sponsored, would appear to agree).”

“It’s worth pointing out that while critics of AA point it as a bit cultlike…to the researchers who believe in its efficacy, there’s actually very little mystery to the process. “We have been able to determine WHY these 12-step facilitation interventions work,” said Kaskutas in an email. “And we have also been able to determine WHY AA works.”

Simply put, “People who self-select to attend AA, or people who are randomized to a 12-step facilitation intervention, end up having people in their social network who are supportive of their abstinence,” she said.

Reams of research show that social networks…are powerful drivers of behavior, so to Kaskutas — who noted that she is an atheist — the focus on AA’s quirks and spiritual undertones misses the point.

“When you think about a mechanism like supportive social networks, or the psychological benefit of helping others… they have to do with the reality of what goes on in AA, with people meeting others in the same boat as they are in, and with helping other people (are but two examples of these mechanisms of action),” she said.”

At the heart of recovery via 12 step groups may be because it “works for a lot of people, simply by connecting them to others going through the same struggles.”

 

 

France - Alcoholic Anonymous celebrates its 75th year

 

 

 

Childhood Maltreatment and later Alcoholism/Addiction

One old timer I know often says two things that I often take issue with – 1. there are as many alcoholisms as alcoholics and that 2. we all come to AA in different boats but end up in the same dock.

Thanks to having a wife in Al Anon I have had the benefit of her insight and from other al-anons who state how remarkably similar we alcoholics are in our behaviour, particularly in dealing/coping with distress and stress, our emotional reactivity and at times immaturity (or so-called defects of character), I disagree that we are so different in our addictive behaviours.

All addictive behaviours from alcoholism, substance addiction, eating disorders to hypersexual disorder seem to be based on an inherent problem with emotion and stress dysregulation.

I believe I have a distress based condition. It results in what appear to be distress based reactions such as perfectionism, distress intolerance and frustration intolerance, normally exemplified in my shouting at my PC when it doesn’t work quickly enough or crashes!

I also believe I have distress based impulsivity, I want that thing, whatever it is, NOW. That anything!

In fact I have noticed when I want something, anything, I end up pathological wanting it in no time at all! It seems then like I NEED it. I too think this is based on distress and heighten stress reactivity.

In fact it is through this pathological wanting that my so-called defects of character that my examples  of emotional dysregulation appear.

If I can’t get what I want, all range of negative emotions spill forth such as intolerance, impatience, arrogance, pride, shame, selfishness etc .  They only appear when I want something and you are getting in the way of me having it!!

So there is a link between my motivation (which is dysregulated due to the effects of chronic stress which turns simple wanting into something more akin to “needing”) and my subsequent emotional dysregulation.

So where does this distress come from? Is it purely the effects of chronic stress dysregulation caused by years of neuro toxic brain damage or does it go back further, into childhood?

I do not think we all have separate alcoholisms, I feel we have remarkably similar reactions to life and these centre on an inherent difficulty regulating stress and emotion.

I also believe we have come to recovery in similar boats. In fact the majority of us have come to recovery in a remarkable similar boat so much so that it would resemble a gigantic ship rather than a boat. That boat is the ship of childhood maltreatment.

Child maltreatment has been frequently identified in the life histories of adolescents and adults in treatment for substance use disorders, as well as in epidemiological studies of risk factors for substance use and abuse.

 Child Maltreatment

One study (1) suggests there is ample evidence exists for higher rates of substance abuse and dependence among maltreated individuals.

In clinical samples undergoing treatment for substance use disorders, between one third and two thirds evince child abuse and neglect histories (Dembo, Dertke, Borders, Washburn, & Schmeidler, 1988Edwall, Hoffman, & Harrison, 1989Pribor & DiWiddie, 1992Schaefer, Sobieragi, & Hollyfield, 1988).

In the US a survey of over 100,000 youth in 6th though 12th grade, Harrison, Fulkerson, and Beebe (1997) Harrison, Fulkerson, and Beebe (1997) found that those reporting either physical or sexual abuse in childhood were from 2 to 4 times more likely to be using drugs than those not reporting abuse; the rates were even higher for youth reporting multiple forms of child maltreatment. Similar findings have been reported by Rodgers et al. (2004) and Moran, Vuchinich, and Hall (2004).

Among youth with Child Protective Services documented maltreatment, Kelly, Thornberry, and Smith (1999) reported one-third higher risk for drug use among those with an abuse history. In a large epidemiological study, Fergusson, Boden, and Horwood (2008) have shown physical abuse and particularly sexual abuse to be related to illicit drug use, as well as abuse and dependence.

Another Study (2) study would suggest the figures are much higher –   data were collected on 178 patients–101 in the United States and 77 in Australia–in treatment for drug/alcohol addiction. The purpose of the study was to determine the degree to which a correlation exists between child abuse/neglect and the later onset of drug/alcohol addiction patterns in the abuse victims. The questionnaire explored such issues as family intactness, parental violence/abuse/neglect, parental drug abuse, sibling relationships and personal physical/sexual abuse histories, including incest and rape. The study determined that 84% of the sample reported a history of child abuse/neglect.

A third study (1) stated that, using the Childhood Trauma Questionnaire-Short Form (CTQ-SF; Bernstein & Fink, 1998; Bernstein et al., 2003) to assess childhood maltreatment in a community sample of active drug users, Medrano, Hatch, Zule, and Desmond (2002) found that 53% of women and 23% of men were sexually abused, 53% of women and 43% of men were physically abused, 58% of women and 39% of men were emotionally abused, 52% of women and 50% of men were physically neglected, and 65% of women and 52% of men were emotionally neglected.

Substance abusers, in addition to having higher rates of childhood maltreatment than members of the general population, have been found to have levels of psychological distress that increase with increasing severity of all types of childhood maltreatment (Medrano et al., 2002). This association is important considering that stress increases an individual’s vulnerability to addiction and addiction relapse (Goeders, 2003; Sinha, 2001;Wills & Hirky, 1996).

There is also evidence that the way in which people cope with stress is related to substance use. For example, researchers have found that greater use of avoidance stress-coping strategies (i.e., disengaging from investing effort to cope with a problem) is related to a greater likelihood of drug use initiation, higher levels of ongoing drug use, and a greater probability of relapse, whereas greater use of active stress-coping strategies (i.e., taking steps to deal with a problem) most consistently functions to protect individuals from substance use initiation and relapse (Wagner, Myers, & McIninch, 1999; Wills & Hirky, 1996).

Childhood maltreatment may influence substance use behavior through its effect on stress and coping. There is emerging evidence that childhood maltreatment may negatively affect the maturation of self-regulatory systems that enable an individual to modulate and tolerate aversive emotional states (Cicchetti & Toth, 2005; Hein, Cohen, & Campbell, 2005). Childhood maltreatment may disrupt neurobiological development and elevate subjective stress by biologically altering the brain’s response to stress (Bugental, 2004;DeBellis, 2002; Heim & Nemeroff, 2001; Heim et al., 2000; Sinha, 2005; Wills & Hirky, 1996). Childhood maltreatment may also affect an individual’s characteristic style of coping with stress so that he or she may be more likely to rely upon maladaptive strategies, such as avoidance of problems, wishful thinking, and social withdrawal, rather than active strategies, such as seeking information and advice from others (Bal, Crombez, Van Oost, & Debourdeaudhuij, 2003; Futa, Nash, Hansen, & Garbin, 2003; Krause, Mendelson, & Lynch, 2003; Leitenberg, Gibson, & Novy, 2004; Thabet, Tischler, & Vostanis, 2004).

Elevated stress and maladaptive coping related to childhood maltreatment may translate to greater substance use behavior by making the coping motives of substance use appear more attractive (Wills & Hirky, 1996). Indeed, substance users commonly report using psychoactive substances such as alcohol, cannabis, and cocaine to cope with stress and regulate affect (Boys, Marsden, & Strang, 2001)

Most cocaine dependent inpatients reported multiple types of childhood maltreatment, and only 15% reported no maltreatment at all, (similar figures to study 2).

“Our findings suggest that the severity of overall childhood maltreatment experienced by recently abstinent cocaine dependent adults has a significant relationship with perceived stress and avoidance coping in adulthood.

Our findings suggest that having a more severe childhood maltreatment history may result in a greater sensitivity to stress…basic coping skills training may not be adequate in decreasing distress and avoidant coping in order to decrease substance use and relapse. Additional interventions that focus on stress tolerance, altering appraisals of stress, stress desensitization, and affect and emotion regulation skills may be of particular benefit to patients with childhood maltreatment histories.

The fact that childhood maltreatment is a preventable phenomenon that occurs early in life and affects psychological functioning well into adulthood makes our findings relevant to clinical practice with children as well. Early identification and treatment of maltreated children may help prevent stress sensitivity or the development of a less adaptive style of coping. Assessment of coping ability and the implementation of coping skills and stress tolerance training may also be indicated for maltreated children in an effort to increase their coping efficacy and decrease their vulnerability to stress later in life.”

I may have been in recovery for a number of years now but coping with stress/distress is still central to my recovery. Dealing with the effects of childhood maltreatment not only via negative self esteem and self schema but in the real sense of coping with every day stress/distress, mainly prompted in my interpersonal relationships (other people!) and with my PC!

 

References

1. Rogosch, F. A., Oshri, A., & Cicchetti, D. (2010). From child maltreatment to adolescent cannabis abuse and dependence: A developmental cascade model.Development and psychopathology, 22(04), 883-897.

2. Cohen, F. S., & Densen-Gerber, J. (1982). A study of the relationship between child abuse and drug addiction in 178 patients: Preliminary results. Child Abuse & Neglect, 6(4), 383-387.

3.  Hyman, S. M., Paliwal, P., & Sinha, R. (2007). Childhood maltreatment, perceived stress, and stress-related coping in recently abstinent cocaine dependent adults. Psychology of Addictive Behaviors, 21(2), 233.

It Works if you Work It!

Alcoholism takes away your life and then kills you.

We look at a study from 8 years ago to show the extent of premature deaths caused by alcoholism and how membership of Alcoholics Anonymous helps in reducing the risk of premature death from alcoholism.

This study (1) of women and men, over 16 years,  observed that those initiating help-seeking careers have better chances of long-term survival. Of the individuals for whom cause of death was known, of the 121 participants known to have died, 76 did so between the 8- and 16-year follow-ups.and 68% died of alcohol-related causes.

Men were more likely to die than were women. When gender was controlled, individuals who were older and unmarried and had more alcohol dependence
symptoms at baseline were more likely to die over the 16-year period.

“It is well documented that the course of alcohol use disorders (AUDs) may end in premature death (Rivara et al., 2004; Room et al., 2005) and …that remission may reduce the risk of premature mortality (Fillmore et al., 2003; Miller, 1999), there is little information about whether an initial course of
professional treatment, or participation in Alcoholics Anonymous (AA), can counteract the connection between AUDs and heightened mortality risk.

To address these issues, we examined mortality in a sample of individuals who had just initiated help-seeking for their AUDs at the start of the study and were followed for 16 years. Specifically, we ascertained the proportions of women and men who died and how these rates compared with matched general population rates…

It Works If You Work It

 

Data on mortality are much more extensive for treated than for untreated individuals with AUDs. Finney and Moos (1991) reviewed long-term studies of mortality among treated individuals. Overall mortality rates ranged from 15% to 42% and were higher when the duration of follow-up was longer (see also Nielsen et al., 2005).

…Among individuals treated for AUDs, mortality rates were higher for men than for women (Feurerlein et al., 1994; Hurt et al., 1996). In addition, in community samples, rates of mortality due to alcohol use were higher in
men than in women (John and Hanke, 2002; Zureik and Ducimetiere, 1996). Premature death due to alcohol abuse or dependence is particularly more likely among men than among women in young and middle-aged groups (Moller-Leimkuhler, 2003)…

…A more severe and longer duration of alcohol abuse predicts premature death (Liskow et al., 2000; Ojesjo, 1981)…. In an 11-year follow-up, Smith et al. (1983) found that women who developed their AUD early and engaged in binge drinking were more likely to die. Consistently, more alcohol consumption and having recognized at a younger age that drinking was a problem were related to more years of life lost to an AUD (Marshall et al., 1994).

…Mackenzie et al. (1986) found that men who were hospitalized for AUDs more frequently were more likely to die over an 8-year follow-up. Inpatient treatment occurring throughout the course of alcoholism may be a marker for a more severe and chronic disorder because such treatment is sought in response to a relapse (Timko et al., 2000). In a study of inpatients with AUDs, de Lint and Levinson (1975) found that death rates were lower in the first 2 years postdischarge than thereafter. They speculated  that intensive outpatient aftercare may delay or prevent the high rate of mortality that often occurs shortly after discharge.

Among individuals treated for AUDs, those who subsequently attended AA were less likely to have died by a 2-year follow-up than those who did not attend (Masudomi et al., 2004)…

… For inpatient care, longer duration appears to be an indicator of greater disorder severity and thus should be associated with higher mortality…However, for outpatient care and help from AA, a longer duration predicts better substance use disorder outcomes and so may  indicate continuing motivation to stop drinking (Moos and Moos, 2003a, 2004a). From this perspective, a longer duration of outpatient treatment or AA affiliation should be associated with lower mortality.

…Furthermore, those who relapsed after treatment were 3 to 5 times more likely to die as those who remained abstinent (Bullock et al., 1992; Feurerlein et al., 1994)…

(This study found)…individuals who are just beginning their help-seeking…have a better chance of long-term survival than do women and men with more chronic disorders.
That is, individuals entering an initial episode of help-seeking may be successful at preventing or reducing the harm associated with excessive drinking that is also potentially causal in death. In contrast, repeated episodes of AUD treatment are often a reflection of the chronic and severe alcoholism known to cause premature death. As other studies have found, men were more likely to die than were women (Feurerlein et al., 1994; Hurt et al., 1996; John and Hanke, 2002; Zureik and Ducimetiere, 1996). Of the individuals who died, over two-thirds died of causes related to alcohol use.

…individuals who were olderand had more alcohol dependence symptoms (Finney and Moos, 1992; Liskow et al., 2000) and were unmarried were
more likely to die over the 16-year observation period.
Alcohol-related mortality tends to be lower among married persons (Agren and Romelsjo, 1992; Lewis et al., 1995)…

keepcomingback

 

…continuous abstinence, had a positive effect on the survival of individuals with AUDs. Studies comparing stable abstinence with reduced frequency and
quantity of abusive drinking found that only stable abstinence prevented a higher mortality risk (Bullock et al., 1992; Gerdner and Berglund, 1997). Our results are consistent with those findings…

 

…Longer duration of AA attendance during the first follow-up year (specifically, attendance for more than 4 months) combined with better 1-year drinking outcomes was associated with a lower likelihood of death in the subsequent 15 years.

Alcoholics Anonymous participation may delay mortality not only by
reducing drinking and drinking-related, including medical,
problems, as outpatient treatment does, but also by increasing social resources and reducing…friendship stressors (Humphreys and Noke, 1997; Kaskutas et al., 2002; Masudomi et al., 2004).

 

References

Timko, C., DeBenedetti, A., Moos, B. S., & Moos, R. H. (2006). Predictors of 16‐year mortality among individuals initiating help‐seeking for an alcoholic use disorder. Alcoholism: Clinical and Experimental Research, 30(10), 1711-1720.